Journal articles on the topic 'Prostaglandins Therapeutic use'
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Jara-Gutiérrez, Álvaro, and Victoriano Baladrón. "The Role of Prostaglandins in Different Types of Cancer." Cells 10, no. 6 (June 13, 2021): 1487. http://dx.doi.org/10.3390/cells10061487.
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The prostaglandins constitute a family of lipids of 20 carbon atoms that derive from polyunsaturated fatty acids such as arachidonic acid. Traditionally, prostaglandins have been linked to inflammation, female reproductive cycle, vasodilation, or bronchodilator/bronchoconstriction. Recent studies have highlighted the involvement of these lipids in cancer. In this review, existing information on the prostaglandins associated with different types of cancer and the advances related to the potential use of them in neoplasm therapies have been analyzed. We can conclude that the effect of prostaglandins depends on multiple factors, such as the target tissue, their plasma concentration, and the prostaglandin subtype, among others. Prostaglandin D2 (PGD2) seems to hinder tumor progression, while prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2α) seem to provide greater tumor progression and aggressiveness. However, more studies are needed to determine the role of prostaglandin I2 (PGI2) and prostaglandin J2 (PGJ2) in cancer due to the conflicting data obtained. On the other hand, the use of different NSAIDs (non-steroidal anti-inflammatory drugs), especially those selective of COX-2 (cyclooxygenase 2), could have a crucial role in the fight against different neoplasms, either as prophylaxis or as an adjuvant treatment. In addition, multiple targets, related to the action of prostaglandins on the intracellular signaling pathways that are involved in cancer, have been discovered. Thus, in depth research about the prostaglandins involved in different cancer and the different targets modulated by them, as well as their role in the tumor microenvironment and the immune response, is necessary to obtain better therapeutic tools to fight cancer.
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Calder, AA. "Prostaglandins as therapy for labour induction or therapeutic abortion." Reproduction, Fertility and Development 2, no. 5 (1990): 553. http://dx.doi.org/10.1071/rd9900553.
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(a) Prostaglandins (especially PGE2) are highly effective for ripening the cervix and inducing labour. If the cervix is already ripe, a small dose of PGE2 may be all that is required to initiate a labour which resembles spontaneous labour as closely as possible. (b) Amniotomy is the central event. Although it is possible for an infant to be born in the caul, i.e. in intact membranes, it is the general rule for the membranes to rupture or to be ruptured during labour. Such rupture leads to heightened activity of endogenous prostaglandins. The timing of amniotomy is crucial. Performed too early, before the cervix is ripe, it may lead to complications. Delayed too late, we may lose the advantage of its uterine sensitizing. (c) Oxytocin is a potent myometrial stimulant if the uterus is primed to respond to it by prostaglandins, either endogenous or exogenous. It must be given intravenously and many mothers find this disagreeable. In most instances of labour induction, a proper combination of prostaglandin therapy and amniotomy may allow the use of oxytocin to be avoided, but it remains the therapy of final resort to carry labour through to delivery if required.
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Toris, Carol B., and Vikas Gulati. "The biology, pathology and therapeutic use of prostaglandins in the eye." Clinical Lipidology 6, no. 5 (October 2011): 577–91. http://dx.doi.org/10.2217/clp.11.42.
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Ragel, Brian T., Randy L. Jensen, and William T. Couldwell. "Inflammatory response and meningioma tumorigenesis and the effect of cyclooxygenase-2 inhibitors." Neurosurgical Focus 23, no. 4 (October 2007): E7. http://dx.doi.org/10.3171/foc-07/10/e7.
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✓In this article the authors discuss the rationale and research supporting the hypothesis that meningioma tumorigenesis may, in part, be driven by overexpression of cyclooxygenase-2 (Cox-2) and that treatment with celecoxib, a selective Cox-2 inhibitor, may hold therapeutic promise. Because therapies for recurrent or aggressive meningiomas (atypical or malignant subtypes) such as chemotherapy and radiotherapy generally offer little therapeutic benefit, interest in targeting Cox-2 has grown. This rate-limiting enzyme of prostaglandin synthesis can be inhibited with nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and celecoxib. Treatment with NSAIDs has been shown to curb the tumorigenic properties of prostaglandins in several cancer models via both Cox-2-dependent and -independent mechanisms. In addition, celecoxib is well tolerated in humans, making its use as a chronic therapy for meningiomas attractive.
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Fattahi, Mohammad Javad, and Abbas Mirshafiey. "Prostaglandins and Rheumatoid Arthritis." Arthritis 2012 (November 7, 2012): 1–7. http://dx.doi.org/10.1155/2012/239310.
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Rheumatoid arthritis (RA) is a chronic, autoimmune, and complex inflammatory disease leading to bone and cartilage destruction, whose cause remains obscure. Accumulation of genetic susceptibility, environmental factors, and dysregulated immune responses are necessary for mounting this self-reacting disease. Inflamed joints are infiltrated by a heterogeneous population of cellular and soluble mediators of the immune system, such as T cells, B cells, macrophages, cytokines, and prostaglandins (PGs). Prostaglandins are lipid inflammatory mediators derived from the arachidonic acid by multienzymatic reactions. They both sustain homeostatic mechanisms and mediate pathogenic processes, including the inflammatory reaction. They play both beneficial and harmful roles during inflammation, according to their site of action and the etiology of the inflammatory response. With respect to the role of PGs in inflammation, they can be effective mediators in the pathophysiology of RA. Thus the use of agonists or antagonists of PG receptors may be considered as a new therapeutic protocol in RA. In this paper, we try to elucidate the role of PGs in the immunopathology of RA.
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Al-Waili, Noori, Khelod Salom, and Ahmad A. Al-Ghamdi. "Honey for Wound Healing, Ulcers, and Burns; Data Supporting Its Use in Clinical Practice." Scientific World JOURNAL 11 (2011): 766–87. http://dx.doi.org/10.1100/tsw.2011.78.
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The widespread existence of unhealed wounds, ulcers, and burns has a great impact on public health and economy. Many interventions, including new medications and technologies, are being used to help achieve significant wound healing and to eliminate infections. Therefore, to find an intervention that has both therapeutic effect on the healing process and the ability to kill microbes is of great value. Honey is a natural product that has been recently introduced in modern medical practice. Honey's antibacterial properties and its effects on wound healing have been thoroughly investigated. Laboratory studies and clinical trials have shown that honey is an effective broad-spectrum antibacterial agent. This paper reviews data that support the effectiveness of natural honey in wound healing and its ability to sterilize infected wounds. Studies on the therapeutic effects of honey collected in different geographical areas on skin wounds, skin and gastric ulcers, and burns are reviewed and mechanisms of action are discussed. (Ulcers and burns are included as an example of challenging wounds.) The data show that the wound healing properties of honey include stimulation of tissue growth, enhanced epithelialization, and minimized scar formation. These effects are ascribed to honey's acidity, hydrogen peroxide content, osmotic effect, nutritional and antioxidant contents, stimulation of immunity, and to unidentified compounds. Prostaglandins and nitric oxide play a major role in inflammation, microbial killing, and the healing process. Honey was found to lower prostaglandin levels and elevate nitric oxide end products. These properties might help to explain some biological and therapeutic properties of honey, particularly as an antibacterial agent or wound healer. The data presented here demonstrate that honeys from different geographical areas have considerable therapeutic effects on chronic wounds, ulcers, and burns. The results encourage the use of honey in clinical practice as a natural and safe wound healer.
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Jarocka-Karpowicz, Iwona, and Agnieszka Markowska. "Therapeutic Potential of Jasmonic Acid and Its Derivatives." International Journal of Molecular Sciences 22, no. 16 (August 5, 2021): 8437. http://dx.doi.org/10.3390/ijms22168437.
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A modern method of therapeutic use of natural compounds that would protect the body are jasmonates. The main representatives of jasmonate compounds include jasmonic acid and its derivatives, mainly methyl jasmonate. Extracts from plants rich in jasmonic compounds show a broad spectrum of activity, i.e., anti-cancer, anti-inflammatory and cosmetic. Studies of the biological activity of jasmonic acid and its derivatives in mammals are based on their structural similarity to prostaglandins and the compounds can be used as natural therapeutics for inflammation. Jasmonates also constitute a potential group of anti-cancer drugs that can be used alone or in combination with other known chemotherapeutic agents. Moreover, due to their ability to stimulate exfoliation of the epidermis, remove discoloration, regulate the function of the sebaceous glands and reduce the visible signs of aging, they are considered for possible use in cosmetics and dermatology. The paper presents a review of literature data on the biological activity of jasmonates that may be helpful in treatment and prevention.
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Breyer, M. D., H. R. Jacobson, and R. M. Breyer. "Functional and molecular aspects of renal prostaglandin receptors." Journal of the American Society of Nephrology 7, no. 1 (January 1996): 8–17. http://dx.doi.org/10.1681/asn.v718.
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The diverse intrarenal effects of the prostaglandins (PG) are mediated by distinct guanine nucleotide regulatory protein (G-protein)-coupled receptors. The cDNA for these receptors have been cloned, their signal transduction mechanisms determined, and their intrarenal distribution mapped. PGE2, the major intrarenal prostaglandin, interacts with at least three distinct E-prostanoid (EP) receptors that are highly expressed in specific regions of the kidney. Each EP receptor not only selectively binds PGE2, but also preferentially couples to different signal transduction pathways, including: stimulation of cAMP generation, via Gq (EP2 and EP4 receptors); inhibition of cAMP generation, via Gi (EP3 receptors); and activation of phosphatidylinositol hydrolysis (EP1 receptor), via one of the Gq family members. Activation of each these EP receptors is responsible for a distinct renal effect of PGE2, including its well-described renal hemodynamic and transport effects along the nephron. Other intrarenal prostanoid receptors include the PGF2 alpha receptor (FP), the thromboxane A2 receptor (TP) and the prostacyclin receptor (IP). Knowledge about localization of these receptors and their affinities for receptor-selective agonists and antagonists should aid in the understanding of renal disease and the development of therapeutic strategies for the use of these prostaglandin analogs in select renal diseases.
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Mistry, C. D., C. J. Lote, R. Gokal, W. J. C. Currie, M. Vandenburg, and N. P. Mallick. "Effects of sulindac on renal function and prostaglandin synthesis in patients with moderate chronic renal insufficiency." Clinical Science 70, no. 5 (May 1, 1986): 501–5. http://dx.doi.org/10.1042/cs0700501.
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1. The renal effects of therapeutic doses of sulindac were studied in nine patients with stable renal insufficiency, mean creatinine clearance 37.0 ± 2.2 ml min−1 1.73 m−2 (range 24.7–54.6 ml min−1 1.73 m−2). 2. Nine days' treatment with sulindac produced a small, but significant, reduction in the mean creatinine clearance (37.0 ± 2.2 to 34.7 ± 2.2 ml min−1 1.73 m−2; P < 0.02) and 99mTc diethylenetriaminepenta-acetate (DTPA) clearance (35.5 ± 3.4 to 31.4 ± 3.6 ml min−1 1.73 m−2; P < 0.02) without altering body weight, effective renal plasma flow [131I]hippuran clearance), plasma renin activity (PRA), 24 h urinary volume or electrolyte excretion. 3. After discontinuation of sulindac, creatinine clearance returned to pretreatment values. 4. In five female patients, pretreatment urinary excretion of the 6-ketoprostaglandin F1α (6-keto-PGF1α), a stable breakdown product of prostacyclin (PGI2), was significantly reduced (P < 0.02) when compared with four healthy controls, whereas prostaglandin E2 (PGE2) was unchanged. Administration of sulindac did not significantly alter the excretion rate of PGE2 or 6-ketoPGF1α in this group of patients. 5. In chronic renal disease with moderate renal impairment, reduced renal prostacyclin synthesis may be an important predisposing factor to the renal toxicity associated with the use of nonsteroidal anti-inflammatory drugs (NSAID). Short term use of sulindac in therapeutic doses does not appear to influence the excretion of prostaglandins and produces only a minor reversible change in renal function; used cautiously it may have advantages over other NSAID in these patients.-
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Bilen Babić, Marijana, Petra Grubešić, Ivana Valković Antić, Renata Gržetić-Lenac, and Maja Merlak. "Nonsteroidal antiinflammatory drugs and treatment of cystoid macular edema." Medicina Fluminensis 55, no. 2 (June 1, 2019): 142–47. http://dx.doi.org/10.21860/medflum2019_218802.
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Nonsteroidal antiinflammatory drugs (NSAIDs) have become a significant therapeutic adjunctive tool in the routine and complicated intraocular surgery. Topical NSAIDs prevent intraoperative miosis, reduce pain, postoperative inflammation and incidence of cystoid macular edema (CME). Although there is no established protocol for prophylaxis of pseudophakic CME, due to the relationship between proinflammatory prostaglandins and CME, using corticosteroids and NSAIDs could prevent CME. NSAIDs have a synergistic antiinflammatory effect with steroids, but can also be used alone when corticosteroid therapy could be harmful. Prospective clinical trials need to define treatment protocol for topical NSAIDs use, due to their powerful influence to prevent perioperative complications.
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Lad, R., and D. Armstrong. "Management of Nonsteroidal Anti-Inflammatory Drug-Induced Gastroduodenal Disease by Acid Suppression." Canadian Journal of Gastroenterology 13, no. 2 (1999): 135–42. http://dx.doi.org/10.1155/1999/715703.
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One major cause of peptic ulceration is the use of nonsteroidal anti-inflammatory drugs (NSAIDs). The precise mechanisms through which NSAIDs cause peptic ulceration are unknown, but the discovery that they reduce the production of ‘cytoprotective’ prostaglandins led to the hypothesis that coadministration of exogenous prostaglandins heals and prevents NSAID-induced gastroduodenal ulcers and other mucosal lesions. Studies using high doses of misoprostol have shown that it does have a protective effect; however, gastrointestinal intolerance of this prostaglandin E2analogue is common. Early indications that acid suppression was effective in the management of NSAID-related peptic ulcers came from studies showing that gastric ulcers could be healed by omeprazole in patients who continued to take NSAIDs. Other studies suggested that acid suppression reduces the incidence of mucosal lesions but that standard dose ranitidine protects only against duodenal lesions. Subsequent studies reported that higher dose H2receptor antagonist therapy can protect against both gastric and duodenal ulcers during continued NSAID therapy. An ideal therapeutic strategy would heal NSAID-related ulcers and prevent the development of new NSAID-related lesions and complications in patients who are unable to discontinue NSAID therapy. A number of recent studies indicate that effective acid-suppressive treatment with the proton pump inhibitor omeprazole can achieve these aims. Overall, data from recent studies show that acid suppression with the proton pump inhibitor omeprazole at a dose of 20 mg daily is the most effective means of healing NSAID-associated gastroduodenal lesions and that it is the most effective prophylactic therapy. In the long run, the role of omeprazole will have to be evaluated with respect to its cost effectiveness compared with other strategies and with respect to the development of less damaging NSAIDs.
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Powell, William S. "Eicosanoid receptors as therapeutic targets for asthma." Clinical Science 135, no. 16 (August 2021): 1945–80. http://dx.doi.org/10.1042/cs20190657.
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Abstract Eicosanoids comprise a group of oxidation products of arachidonic and 5,8,11,14,17-eicosapentaenoic acids formed by oxygenases and downstream enzymes. The two major pathways for eicosanoid formation are initiated by the actions of 5-lipoxygenase (5-LO), leading to leukotrienes (LTs) and 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE), and cyclooxygenase (COX), leading to prostaglandins (PGs) and thromboxane (TX). A third group (specialized pro-resolving mediators; SPMs), including lipoxin A4 (LXA4) and resolvins (Rvs), are formed by the combined actions of different oxygenases. The actions of the above eicosanoids are mediated by approximately 20 G protein-coupled receptors, resulting in a variety of both detrimental and beneficial effects on airway smooth muscle and inflammatory cells that are strongly implicated in asthma pathophysiology. Drugs targeting proinflammatory eicosanoid receptors, including CysLT1, the receptor for LTD4 (montelukast) and TP, the receptor for TXA2 (seratrodast) are currently in use, whereas antagonists of a number of other receptors, including DP2 (PGD2), BLT1 (LTB4), and OXE (5-oxo-ETE) are under investigation. Agonists targeting anti-inflammatory/pro-resolving eicosanoid receptors such as EP2/4 (PGE2), IP (PGI2), ALX/FPR2 (LXA4), and Chemerin1 (RvE1/2) are also being examined. This review summarizes the contributions of eicosanoid receptors to the pathophysiology of asthma and the potential therapeutic benefits of drugs that target these receptors. Because of the multifactorial nature of asthma and the diverse pathways affected by eicosanoid receptors, it will be important to identify subgroups of asthmatics that are likely to respond to any given therapy.
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Ben-Efraim, S. "Cancer immunotherapy: potential involvement of mediators." Mediators of Inflammation 6, no. 3 (1997): 163–73. http://dx.doi.org/10.1080/09629359791659.
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The description of a cell-free soluble anti-tumour factor by Carswellet al. in 1975 (Proc Natl Acad Sci USA, 72: 3666–3670) was followed by a long series of experimental and clinical investigations into the role of cell-free mediators in cancer immunotherapy. These investigations included research on the effects of macrophage–derived eicosanoids (cycloxygenase and lipoxygenase derivates of arachidonic acid) and of monokines such as tumour necrosis factor-α, interleukin-1 and granulocyte–monocyte–macrophage–colony stimulating factor) and of lymphocyte products: interleukins and interferons. The investigations yielded information on the effects of various factors on macrophage and T-cell activationin vitro, determination of direct anti-tumour properties on animal and human tumour cellsin vitroand on therapeutic effectiveness in tumour-bearing individuals either alone or in combination with other therapeutic factors and their production by tumour cells. During recent years much effort has been dedicated towards the use of the tumour cells transfected with cytokine genes in the preparation of cancer vaccines. Cycloxygenase products (prostaglandins) were usually assumed to inhibit expression of anti-tumour activity by macrophages and an increase in their production in cancer patients was considered as a poor prognostic index. Lipoxygenase (leukotrienes) products were assumed to exhibit antitumour activity and to induce production of IL-1 by macrophages. Interleukins 2, 4, 6, 7, 12 and the interferons were extensively tested for their therapeutic effectiveness in experimental tumour models and in cancer clinical trials. The general conclusion on the use of cell-free mediators for cancer immunotherapy is that much still has to be done in order to assure effective and reproducible therapeutic effectiveness for routine use in the treatment of human neoplasia.
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Belton, Orina, and Desmond J. Fitzgerald. "Cyclooxygenase isoforms and atherosclerosis." Expert Reviews in Molecular Medicine 5, no. 9 (March 7, 2003): 1–18. http://dx.doi.org/10.1017/s1462399403005842.
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Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used in the treatment of arthritis and pain. However, their long-term use is limited by gastrointestinal (GI) side effects such as gastric ulcers. NSAIDs act by inhibiting an enzyme called cyclooxygenase. Cyclooxygenase (COX) catalyses the generation of prostaglandins from arachidonic acid. Two isoforms of the enzyme exist – COX-1 and COX-2 – both of which are targets for NSAIDs. Although they are associated with GI toxicity, NSAIDs have important antithrombotic and anti-inflammatory effects. The GI injury has been attributed to COX-1 inhibition and the anti-inflammatory effects to COX-2 inhibition. As COX-2 is traditionally viewed as an inducible enzyme, selective inhibition of COX-2 by ‘coxibs’ (selective COX-2 inhibitors) has been employed to achieve anti-inflammatory and analgesic effects without GI side effects. However, recently there have been suggestions that chronic administration of coxibs might increase the risk of cardiovascular events, such as atherosclerosis, compared with traditional NSAIDs. In vascular disease, there is increased expression of both COX-1 and COX-2, resulting in enhanced prostaglandin generation. The specific role of COX-1 and COX-2 in vascular regulation is still unknown but such knowledge is essential for the effective use of coxibs. Although more evidence is pointing to selective COX-1 inhibition as a therapeutic measure in inflammatory atherosclerosis, there are some studies that suggest that inhibition of COX-2 might have a potential benefit on atherosclerosis.
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Trigub, Anastasia V., and Aleksandr A. Stepchenko. "Unique cytoprotective properties of Rebamipide: review of basic and clinical research." Курский научно-практический вестник «Человек и его здоровье», no. 3 (September 2020): 4–10. http://dx.doi.org/10.21626/vestnik/2020-3/01.
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The article presents current experimental and clinical data on the effectiveness and safety of the use of the drug Rebamipide in the therapy of erosive and ulcerative lesions of the gastrointestinal tract (GIT), including those caused by Helicobacter pylori infection, non-steroidal anti-inflammatory drugs (NSAIDs), aspirin, endoscopic submucosal dissection for early gastric cancer For a long time, proton pump inhibitors (PPIs) were the only means of drug prevention of these complications. However, PPIs are effective only for the prevention and treatment of pathology of the upper gastrointestinal tract, but not for pathology of the small intestine. With NSAIDs, gastro- and enteropathies, it is advisable to use drugs that can increase the production of prostaglandins and mucus, restore the permeability of the intestinal epithelium, and have anti-inflammatory and antioxidant effects. Today, doctors have a new instrument for protecting the gastrointestinal mucosa - Rebamipide. This drug is a unique cytoprotector that stimulates the production of endogenous prostaglandins and mucus glycoproteins, inhibits reactive oxygen species, the production of inflammatory cytokines and chemokines, and inhibits the activation of neutrophils. In addition, Rebamipide stimulates the synthesis of epidermal growth factor, vascular endothelial growth factor, and nitric oxide. These properties make it possible to use it in various fields of medicine: gastroenterology, ophthalmology, chemotherapy, rheumatology, and endoscopy. Currently, active developments are underway to create new dosage forms of the drug and search for new therapeutic targets. The aim of this study was to analyze the available publications on clinical and experimental studies of the efficacy and safety of using Rebamipide in the treatment of a wide range of pathological conditions.
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Hladkykh, Feydor V. "Preventive and therapeutic strategies of pharmaco-correction gastropathy induced by nonsteroidal anti-inflammatory drugs." Reviews on Clinical Pharmacology and Drug Therapy 15, no. 4 (December 15, 2017): 14–23. http://dx.doi.org/10.17816/rcf15414-23.
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Today the problem of prevention and treatment of gastropathy associated with nonsteroidal anti-inflammatory drugs has not lost its relevance. In order to reduce the ulcerogenicity of non-steroidal anti-inflammatory drugs, it is classically accepted to supplement the therapy scheme with preparations of other pharmacological groups - antacids, alginates, M-cholinoblockers, gastrin receptor antagonists, H2-histamine blockers, proton pump inhibitors, synthetic analogues of prostaglandins or stimulators of their synthesis, reparants, gastroprotectors. Nowadays, it was suggested I was suggested the use of drugs which have pharmacological properties polyvector (vinboron, thiotriazoline et al.). Also, the scientists started of combined preparations “NSAIDs + drugs other pharmacological groups” - indotril (indomethacin + thiotriazoline) diklokor (diclofenac + quercetin) Artrotek (diclofenac sodium + misoprostol) dueksis (ibuprofen + famotidine) vimovo (naproxen + esomeprazole) aksorid (ketoprofen + omeprazole) tioaspekard (thiotriazoline + ACK) aspifat (ACK + sucralfate), Alka-Zelttser® (ACK + sodium bicarbonate), and others. The second direction is preventing and improving NSAID gastrotoxicity protrudes improving existing non-steroidal drugs - modification of gaseous molecules (NO, H2S, CO), amino acid derivatives, modulators “effector function” of afferent terminals n. vagus (amtolmetina guatsil) то pairing with nanoparticles biometals (Zn-ibuprofen, Zn-naproxen, Zn-indomethacin). (For citation: Hladkykh FV. Preventive and therapeutic strategies of pharmaco-correction gastropathy induced by nonsteroidal anti-inflammatory drugs. Reviews on Clinical Pharmacology and Drug Therapy. 2017;15(4):14-23. doi: 10.17816/RCF15414-23).
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Jahnavi, Kasturi, Palla Pavani Reddy, Bakshi Vasudha, and Boggula Narender. "Non-steroidal anti-inflammatory drugs: an overview." Journal of Drug Delivery and Therapeutics 9, no. 1-s (February 15, 2019): 442–48. http://dx.doi.org/10.22270/jddt.v9i1-s.2287.
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Non-steroidal anti-inflammatory drugs (NSAIDs) including both traditional non-selective NSAIDs and the selective cyclooxygenase (COX)-2 inhibitors, are widely used for their anti-inflammatory and analgesic effects. NSAIDs are a necessary choice in pain management because of the integrated role of the COX path way in the generation of inflammation and in the biochemical recognition of pain. NSAIDs are the competitive inhibitors of cyclooxygenase (COX), the enzyme which mediates the bioconversion of arachidonic acid to inflammatory prostaglandins (PGs). Their use is associated with the side effects such as gastrointestinal and renal toxicity. They are the most commonly employed first line drugs for all these conditions and many others-like musculoskeletal trauma, minor aches and pains, and dysmenorrhoea. The therapeutic anti-inflammatory action of NSAIDs is produced by the inhibition of COX-2, while the undesired side effects arise from inhibition of COX-1 activity. Thus, it was though those more selective COX-2 inhibitors would have reduced side effects. Based upon a number of selective COX-2 inhibitors (Rofecoxib, Celecoxib etc.) were developed as safer NSAIDs with improved gastric safety profile. Several newer applications like prophylaxis of stroke with aspirin are now common place. Use of these drugs for the prophylaxis of conditions like Alzheimer’s disease and colorectal cancer is being evaluated. Unfortunately, they have several toxicities ranging from minor heartburn to severe gastrointestinal haemorrhage and perforation. Therefore, newer NSAIDs have been introduced in recent years to circumvent this problem. In preliminary studies, these have shown better safety, efficacy, and tolerability but the full spectrum of adverse reactions of these drugs is yet to be fully known. This review can be used for further research as well as clinical purpose.
Keywords: Non-steroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase inhibitors, prostaglandins, aspirin.
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Alegbeleye, Bamidele Johnson, Oke-Oghene Philomena Akpoveso, Adewale James Alegbeleye, Rana Kadhim Mohammed, and Eduardo Esteban-Zubero. "The Novel Aspirin as Breakthrough Drug for COVID-19: A Narrative Review." Iberoamerican Journal of Medicine 2, no. 4 (August 3, 2020): 335–50. http://dx.doi.org/10.53986/ibjm.2020.0058.
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Introduction: Aspirin has justifiably been called the first miracle drug. In this article, we highlight the history of Aspirin, a novel mechanism of action, and its use in cardiovascular and other diseases. Also included is a brief statement of emerging new applications. Objective: We highlight principal mechanisms by which Aspirin inhibits acute inflammation and alters platelet-biology; therefore, hypothesized that Aspirin might prove highly beneficial as a novel therapeutic drug for combating severe acute inflammation and thrombosis associated with the cytokine storm in COVID -19 patients. The communiqué also suggests possible strategies for maximizing the gain of Aspirin as a wonder-drug of the future. Discussion: Interestingly, some fascinating studies demonstrated Aspirin's superior benefits with dangerous side effects. Aspirin inhibits COX-1 (cyclooxygenase-1). Its impact on COX-2 is more delicate because it “turns off” COX-2's production of prostaglandins but “switches on” the enzymatic ability to produce novel protective lipid mediators. The established mechanism of action of Aspirin is the inhibition of prostaglandin synthesis. However, further evidence showed that aspirin-elicited nitric oxide exerts anti-inflammatory effects in the microcirculation by inhibiting leukocyte– endothelium interactions. Interestingly, aspirin-triggered lipoxin formation may provide a novel mechanism underlying Aspirin's clinical benefits. Interestingly, Aspirin reduces the risk of a cardiovascular event by about 30 percent. Also, Aspirin has been associated with a reduced risk of colorectal cancer, and possibly a few other digestive tract cancers. Conclusion: The current emerging interest is to conduct further study to provide evidence for Aspirin as the novel therapeutic drug for combating severe acute inflammation and thrombosis associated with the cytokine storm in COVID-19 patients. Besides, the most wanted is The RECOVERY II (Randomized Evaluation of COVID-19 Therapy II) trial to be established as a randomized clinical trial to test the effectiveness of low-dose Aspirin as an anti-inflammatory and antithrombotic treatment in COVID-19 patients.
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Akarasereenont, Pravit, Kitirat Techatrisak, Sirikul Chotewuttakorn, and Athiwat Thaworn. "The Induction of Cyclooxygenase-2 in IL-1β-Treated Endothelial Cells is Inhibited by Prostaglandin E2 through cAMP." Mediators of Inflammation 8, no. 6 (1999): 287–94. http://dx.doi.org/10.1080/09629359990298.
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Prostaglandins (PGS) have numerous cardiovascular and inflammatory effects. Cyclooxygenase (COX), which exists as COX-1 and COX-2 isoforms, is the first enzyme in the pathway in which arachidonic acid is converted to PGs. Prostaglandin E2 (PGE2) exerts a variety of biological activities for the maintenance of local homeostasis in the body. Elucidation of PGE2 involvement in the signalling molecules such as COX could lead to potential therapeutic interventions. Here, we have investigated the effects of PGE2 on the induction of COX-2 in human umbilical vein endothelial cells (HUVEC) treated with interleukin-1β (IL-1β 1 ng/ml). COX activity was measured by the production of 6-keto-PGF1α, PGE2, PGF2α and thromboxane B2 (TXB2) in the presence of exogenous arachidonic acids (10 μM for 10 min) using enzyme immunoassay (EIA). COX-1 and COX-2 protein was measured by immunoblotting using specific antibody. Untreated HUVEC contained only COX-1 protein while IL-1β treated HUVEC contained COX-1 and COX-2 protein. PGE2 (3 μM for 24 h) did not affect on COX activity and protein in untreated HUVEC. Interestingly, PGE2 (3 μM for 24 h) can inhibit COX-2 protein, but not COX-1 protein, expressed in HUVEC treated with IL1 β. This inhibition was reversed by coincubation with forskolin (100 μM). The increased COX activity in HUVEC treated with IL-1β was also inhibited by PGE2 (0.03, 0.3 and 3 μM for 24 h) in a dose-dependent manner. Similarly, forskolin (10, 50 or 100 μM) can also reverse the inhibition of PGE2 on increased COX activity in IL-1β treated HUVEC. The results suggested that (i) PGE2 can initiate negative feedback regulation in the induction of COX-2 elicited by IL-1β in endothelial cells, (ii) the inhibition of PGE2 on COX-2 protein and activity in IL-1β treated HUVEC is mediated by cAMP and (iii) the therapeutic use of PGE2 in the condition which COX-2 has been involved may have different roles.
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Pakhomova, I. G. "Features of therapeutic correction of GERD: focus on cytoprotection (with a clinical case)." Meditsinskiy sovet = Medical Council, no. 21-1 (January 6, 2022): 87–92. http://dx.doi.org/10.21518/2079-701x-2021-21-1-87-92.
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Тo date, the possible links of the pathogenesis of this disease have been well studied and described, which predetermine certain approaches to the treatment of various variants of gastroesophageal reflux disease (GERD). Effective drug therapy for GERD includes proton pump inhibitors (PPI). However, PPI monotherapy is not always effective. One approach is to increase the PPI dose. At the same time, combination therapy with the addition of drugs that affect the protective properties of the esophageal mucosa seems to be more rational. It is known that in the development of GERD, the violation of cytoprotection of the esophageal mucosa is one of the key links in pathogenesis. Consequently, the issue of combination therapy of PPIs with drugs that increase the protective properties of the mucous barrier along with acid suppression becomes relevant. An example of such an approach is the appointment of rebamipide, the action of which is to regulate the synthesis of prostaglandins through COX-2 mediated mechanisms, influence on endothelial growth factor, increase the expression of tight intercellular contact proteins in epithelial cells of the mucous membrane, reduce the level of interleukin-8 and free oxygen radicals, directed to protect the mucous membrane of the gastrointestinal tract and restore its natural barrier properties. The effectiveness of the combination of PPI and rebamipide contributes to a greater regression of complaints in patients with GERD and a lower frequency of disease relapses than with PPI monotherapy. This article provides a review of the literature on the features of GERD therapy, primarily with an emphasis on the correction of the cytoprotective properties of the esophageal mucosa, including against the background of the use of nonsteroidal anti-inflammatory drugs (NSAID), and a clinical case analysis with a discussion of rational pharmacological correction.
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Varela-Chinchilla, Carlos Daniel, Daniela Edith Sánchez-Mejía, and Plinio A. Trinidad-Calderón. "Congenital Heart Disease: The State-of-the-Art on Its Pharmacological Therapeutics." Journal of Cardiovascular Development and Disease 9, no. 7 (June 26, 2022): 201. http://dx.doi.org/10.3390/jcdd9070201.
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Congenital heart disease is one of the most common causes of death derived from malformations. Historically, its treatment has depended on timely diagnosis and early pharmacological and surgical interventions. Survival rates for patients with this disease have increased, primarily due to advancements in therapeutic choices, but mortality remains high. Since this disease is a time-sensitive pathology, pharmacological interventions are needed to improve clinical outcomes. Therefore, we analyzed the applications, dosage, and side effects of drugs currently used for treating congenital heart disease. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, and potassium-sparing diuretics have shown a mortality benefit in most patients. Other therapies, such as endothelin receptor antagonists, phosphodiesterase-5 inhibitors, prostaglandins, and soluble guanylyl cyclase stimulators, have benefited patients with pulmonary artery hypertension. Likewise, the adjunctive symptomatic treatment of these patients has further improved the outcomes, since antiarrhythmics, digoxin, and non-steroidal anti-inflammatory drugs have shown their benefits in these cases. Conclusively, these drugs also carry the risk of troublesome adverse effects, such as electrolyte imbalances and hemodynamic compromise. However, their benefits for survival, symptom improvement, and stabilization outweigh the possible complications from their use. Thus, cases must be assessed individually to accurately identify interventions that would be most beneficial for patients.
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Clower, Lauren, Taylor Fleshman, Werner J. Geldenhuys, and Nalini Santanam. "Targeting Oxidative Stress Involved in Endometriosis and Its Pain." Biomolecules 12, no. 8 (July 29, 2022): 1055. http://dx.doi.org/10.3390/biom12081055.
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Endometriosis is a common gynecological disorder seen in women and is characterized by chronic pelvic pain and infertility. This disorder is becoming more prevalent with increased morbidity. The etiology of endometriosis remains to be fully elucidated, which will lead to improved therapeutic options. In this review, we will evaluate the biochemical mechanisms leading to oxidative stress and their implication in the pathophysiology of endometriosis, as well as potential treatments that target these processes. A comprehensive exploration of previous research revealed that endometriosis is associated with elevated reactive oxygen species and oxidation products, decreased antioxidants and detoxification enzymes, and dysregulated iron metabolism. High levels of oxidative stress contributed to inflammation, extracellular matrix degradation, angiogenesis, and cell proliferation, which may explain its role in endometriosis. Endometriosis-associated pain was attributed to neurogenic inflammation and a feed-forward mechanism involving macrophages, pro-inflammatory cytokines, and pain-inducing prostaglandins. N-acetylcysteine, curcumin, melatonin, and combined vitamin C and E supplementation displayed promising results for the treatment of endometriosis, but further research is needed for their use in this population.
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Gargya, Isha, Baljeet Singh, and Sanjay Talnia. "NSAIDS (Non- Steroidal Anti- Inflammatory Drugs)- Their Effects and Side Effects in Orthodontic Therapy- A Review." Dental Journal of Advance Studies 05, no. 01 (April 2017): 008–13. http://dx.doi.org/10.1055/s-0038-1672075.
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AbstractOrthodontic tooth movement(OTM) is a complex process involving physiologic processes resulting in remodelling changes in the paradental tissues which are essential in orthodontic correction of tooth position. Medications have an influence on tooth movement and information on their consumption is essential to discuss treatment planning with patients. Various drugs either prescribed by the clinician or consumed by the patients enter the circulation and may be inhibitory, additive or synergise with the movement of teeth. Tooth movement through the remeodelling of bone is regulated by prostaglandins(PG) which play a direct role in bone resorption and is adversely affected by the use of NSAIDs(Non- Steroidal anti-inflammatory drugs) with research and clinical experience suggesting that their use slows down tooth movement due to a reduction in the number of osteoclastic cells. Since tooth movement is the key principle behind orthodontic treatment, any factor affecting the biologic response towards applied mechanical force is deemed to affect orthodontic treatment duration as well as efficacy. The purpose of this review article is to update the clinician on the roleof most commonly used pharmaceutical drugs capable of affecting bone metabolism and rate of orthodontic tooth movement so that best therapeutic strategy can be formulated for an individual.
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Medeiros, Maria Alice Miranda Bezerra, Mariana Gama e Silva, Jackson de Menezes Barbosa, Érica Martins de Lavor, Tiago Feitosa Ribeiro, Cícero André Ferreira Macedo, Luiz Antonio Miranda de Souza Duarte-Filho, et al. "Antinociceptive and anti-inflammatory effects of hydrazone derivatives and their possible mechanism of action in mice." PLOS ONE 16, no. 11 (November 24, 2021): e0258094. http://dx.doi.org/10.1371/journal.pone.0258094.
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Pain and inflammation are unpleasant experiences that usually occur as a result of tissue damage. Despite the number of existing analgesic drugs, side effects limit their use, stimulating the search for new therapeutic agents. In this sense, five hydrazone derivatives (H1, H2, H3, H4, and H5), with general structure R1R2C = NNR3R4, were synthesized with molecular modification strategies. In this paper, we describe the ability of hydrazone derivatives to attenuate nociceptive behavior and the inflammatory response in mice. Antinociceptive activity was evaluated through acetic acid-induced writhing and formalin-induced nociception tests. In both experimental models, the hydrazone with the greatest potency (H5) significantly (p < 0.05) reduced nociceptive behavior. Additionally, methods of acute and chronic inflammation induced by different chemicals (carrageenan and histamine) were performed to evaluate the anti-inflammatory effect of H5. Moreover, molecular docking analysis revealed that H5 can block the COX-2 enzyme, reducing arachidonic acid metabolism and consequently decreasing the production of prostaglandins, which are important inflammatory mediators. H5 also changes locomotor activity. In summary, H5 exhibited relevant antinociceptive and anti-inflammatory potential and acted on several targets, making it a candidate for a new multi-target oral anti-inflammatory drug.
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Vernieri, Ermelinda, Isabel Gomez-Monterrey, Ciro Milite, Paolo Grieco, Simona Musella, Alessia Bertamino, Ilaria Scognamiglio, et al. "Design, Synthesis, and Evaluation of New Tripeptides as COX-2 Inhibitors." Journal of Amino Acids 2013 (February 26, 2013): 1–7. http://dx.doi.org/10.1155/2013/606282.
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Cyclooxygenase (COX) is a key enzyme in the biosynthetic pathway leading to the formation of prostaglandins, which are mediators of inflammation. It exists mainly in two isoforms COX-1 and COX-2. The conventional nonsteroidal anti-inflammatory drugs (NSAIDs) have gastrointestinal side effects because they inhibit both isoforms. Recent data demonstrate that the overexpression of these enzymes, and in particular of cyclooxygenases-2, promotes multiple events involved in tumorigenesis; in addition, numerous studies show that the inhibition of cyclooxygenases-2 can delay or prevent certain forms of cancer. Agents that inhibit COX-2 while sparing COX-1 represent a new attractive therapeutic development and offer a new perspective for a further use of COX-2 inhibitors. The present study extends the evaluation of the COX activity to all 203 possible natural tripeptide sequences following a rational approach consisting in molecular modeling, synthesis, and biological tests. Based on data obtained from virtual screening, only those peptides with better profile of affinity have been selected and classified into two groups called S and E. Our results suggest that these novel compounds may have potential as structural templates for the design and subsequent development of the new selective COX-2 inhibitors drugs.
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Velentgas, Priscilla, Reinee Sheffield, Beth L. Nordstrom, Eric Johnson, Thy Do, Sherry M. Mentor, and John D. Seeger. "Persistence with Medications in Glaucoma Management, Hypertension, and Dyslipidemia." Journal of Pharmacy Technology 23, no. 4 (July 2007): 221–31. http://dx.doi.org/10.1177/875512250702300406.
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Objective: To summarize pharmacy database studies of persistence with ocular hypotensives and review the literature of adherence with 2 additional classes of medication—antihypertensives and antihyperlipidemics—comparing methods used to analyze adherence in the 3 treatment areas. Data Sources: A search of MEDLINE (1990–2004) was conducted, using search terms designed to identify English-language articles describing adherence or persistence with any of the 3 drug classes of interest. Study Selection and Data Extraction: All articles identified through MEDLINE were reviewed and screened for use of an automated pharmacy database as an information source, quantitative results provided, and follow-up duration of at least 90 days. Details of methods used to estimate adherence or persistence and estimates of persistence with ocular hypotensive therapy, antihypertensives, and lipid-lowering agents were extracted. Data Synthesis: All studies describing the use of ocular hypotensives, and the majority of studies in the other treatment areas, identified inception cohorts of drug initiators. Use of survival analysis techniques to analyze adherence to medication therapy was less common in the hypertension and hyperlipidemia treatment adherence literature than in literature about glaucoma. In the treatment of hypertension, use of angiotensin II receptor antagonists or angiotensin-converting enzyme inhibitors was associated with higher levels of adherence. Statins in treatment of hyperlipidemia and topical prostaglandins as ocular hypotensive medications were also associated with higher levels of adherence. Conclusions: Findings regarding the relative superiority of specific drug classes were consistent within each therapeutic area, with less consistency in identifying other predictors of adherence. Increased use of survival analysis in future studies of persistence might improve comparability of results across studies.
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Nakamura, Masato, Akiyoshi Shinohara, Toshihide Onikubo, Kumi Nakamura, Harumi Kamikawa, Kyota Oda, and Katsunori Tauchi. "Efficacy of rebamipide-gargle for chemotherapy-induced oral mucositis." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 9637. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9637.
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9637 Background: Chemotherapy-induced oral mucositis (CIOM) is a severe adverse event resulting from cancer chemotherapy, and causes severe pain which impacts eating, nutrition, infection and overall quality of life. CIOM can result in unplanned treatment interruptions including dose reduction or treatment delay. Toxic free radicals and several pro-inflammatory cytokines produced by anti-cancer drugs have been reported to correlate with CIOM. Rebamipid, an endogenous inducer of prostaglandins, is widely used for gastric ulcers and gastritis in Asia. It has been shown to increase gastric endogenous prostaglandin E2 and I2, to promote gastric epithelial mucin, to behave as an oxygen–free radical scavenger, and to have other anti-inflammatory actions. In this study, we made a rebamipide gargle using rebamipide and ultrahydrogel, which is added for mucosal protection and to sustain the rebamipide on oral mucosa for a long time. Methods: The objective of this study is to evaluate the efficacy of the rebamipide gargle in relieving CIOM. Each 300ml of rebamipide gargle is made by combining rebamipide 600mg, high molecular weight polyethylene oxide 3g, carrageenin 1.2g, pineapple flavor and water. Patients were instructed to use the rebamipide gargle 5-6 times a day. The severity of CIOM was assessed according to the National Cancer Institute Common TerminologyCriteria for Adverse Events (CTCAE version 4.0). Results: From November 2009 to December 2012, 175 patients with CIOM were enrolled in this study (colorectal cancer 95 patients, breast cancer 32, gastric cancer 22, lung cancer 14, and other cancers 12). The patients’ CTCAE grades (3/2/1/0) changed from (n=13/64/98/0) to (0/10/103/62) respectively after initiation of rebamipide gargle (p<.01; paired t test). A decrease in CTCAE was observed in 142 patients (81.1%) including 62 patients (35.4%) achieving grade 0. The mean duration to best response was 14 days (range: 1-49), and rebamipide gargle was continued 42 days (range: 5-970).There were no unexpected safety events. Conclusions: Rebamipide gargle was well tolerated and demonstrated significant therapeutic response for CIOM.
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Kulkarni, Abhay P., and Himanshu A. Bendrey. "Systemic enzyme therapy with trypsin, bromelain and rutoside in the management of arthritis: an overview." International Journal of Research in Orthopaedics 7, no. 5 (August 25, 2021): 1062. http://dx.doi.org/10.18203/issn.2455-4510.intjresorthop20213392.
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<p class="abstract">Chronic arthritis, including osteoarthritis and rheumatoid arthritis, is a growing major public health problem leading to disability and reduced quality of life. Analgesic and anti-inflammatory drugs form the mainstay of treatment for chronic arthritis. The protracted use of the conventional medications for their management is fraught with shortcomings, including safety concerns. Proteolytic enzymes and antioxidant combinations have been used empirically, since ages, in many of these conditions. There is a growing body of evidence indicating the beneficial effects exerted by the individual ingredients and their combinations on the pathophysiology of arthritis. The analgesic, anti-inflammatory, anti-edematous, anti-thrombotic and anti-oxidant properties of these substances have been demonstrated in multiple in vitro and animal models. Furthermore, the therapeutic use of proteolytic enzyme-antioxidant combination is also supported by clinical trials in arthritis and related disorders. Such studies have mostly been carried out on preparations consisting of combinations of trypsin, bromelain and rutoside. The results of various studies (placebo-controlled and comparisons with nonsteroidal anti-inflammatory (NSAIDs) drugs) in patients with arthritis suggest that oral therapy with such enzyme-antioxidant combination produces improvement in all major clinical parameters like swelling, pain and joint stiffness and have comparable efficacy to NSAIDs. Some clinical studies also evaluated their effect on biochemical markers like cytokines, interferons and prostaglandins and reported remarkable improvements. The overall data also indicates that the tolerability of the enzyme-antioxidant combination is better than conventional therapies.</p>
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Krishnan, Aruna V., and David Feldman. "Molecular pathways mediating the anti-inflammatory effects of calcitriol: implications for prostate cancer chemoprevention and treatment." Endocrine-Related Cancer 17, no. 1 (March 2010): R19—R38. http://dx.doi.org/10.1677/erc-09-0139.
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Calcitriol, the hormonally active form of vitamin D, exerts multiple anti-proliferative and pro-differentiating actions including cell cycle arrest and induction of apoptosis in many malignant cells, and the hormone is currently being evaluated in clinical trials as an anti-cancer agent. Recent research reveals that calcitriol also exhibits multiple anti-inflammatory effects. First, calcitriol inhibits the synthesis and biological actions of pro-inflammatory prostaglandins (PGs) by three mechanisms: i) suppression of the expression of cyclooxygenase-2, the enzyme that synthesizes PGs; ii) up-regulation of the expression of 15-hydroxyprostaglandin dehydrogenase, the enzyme that inactivates PGs; and iii) down-regulation of the expression of PG receptors that are essential for PG signaling. The combination of calcitriol and nonsteroidal anti-inflammatory drugs results in a synergistic inhibition of the growth of prostate cancer (PCa) cells and offers a potential therapeutic strategy for PCa. Second, calcitriol increases the expression of mitogen-activated protein kinase phosphatase 5 in prostate cells resulting in the subsequent inhibition of p38 stress kinase signaling and the attenuation of the production of pro-inflammatory cytokines. Third, calcitriol also exerts anti-inflammatory activity in PCa through the inhibition of nuclear factor-κB signaling that results in potent anti-inflammatory and anti-angiogenic effects. Other important direct effects of calcitriol as well as the consequences of its anti-inflammatory effects include the inhibition of tumor angiogenesis, invasion, and metastasis. We hypothesize that these anti-inflammatory actions, in addition to the other known anti-cancer effects of calcitriol, play an important role in its potential use as a therapeutic agent for PCa. Calcitriol or its analogs may have utility as chemopreventive agents and should be evaluated in clinical trials in PCa patients with early or precancerous disease.
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Manneck, David, Gisela Manz, Hannah-Sophie Braun, Julia Rosendahl, and Friederike Stumpff. "The TRPA1 Agonist Cinnamaldehyde Induces the Secretion of HCO3− by the Porcine Colon." International Journal of Molecular Sciences 22, no. 10 (May 14, 2021): 5198. http://dx.doi.org/10.3390/ijms22105198.
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A therapeutic potential of the TRPA1 channel agonist cinnamaldehyde for use in inflammatory bowel disease is emerging, but the mechanisms are unclear. Semi-quantitative qPCR of various parts of the porcine gastrointestinal tract showed that mRNA for TRPA1 was highest in the colonic mucosa. In Ussing chambers, 1 mmol·L−1 cinnamaldehyde induced increases in short circuit current (ΔIsc) and conductance (ΔGt) across the colon that were higher than those across the jejunum or after 1 mmol·L−1 thymol. Lidocaine, amiloride or bumetanide did not change the response. The application of 1 mmol·L−1 quinidine or the bilateral replacement of 120 Na+, 120 Cl− or 25 HCO3− reduced ΔGt, while the removal of Ca2+ enhanced ΔGt with ΔIsc numerically higher. ΔIsc decreased after 0.5 NPPB, 0.01 indometacin and the bilateral replacement of 120 Na+ or 25 HCO3−. The removal of 120 Cl− had no effect. Cinnamaldehyde also activates TRPV3, but comparative measurements involving patch clamp experiments on overexpressing cells demonstrated that much higher concentrations are required. We suggest that cinnamaldehyde stimulates the secretion of HCO3− via apical CFTR and basolateral Na+-HCO3− cotransport, preventing acidosis and damage to the epithelium and the colonic microbiome. Signaling may involve the opening of TRPA1, depolarization of the epithelium and a rise in PGE2 following a lower uptake of prostaglandins via OATP2A1.
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Vincendeau, Philippe, and Bernard Bouteille. "Immunology and immunopathology of African trypanosomiasis." Anais da Academia Brasileira de Ciências 78, no. 4 (December 2006): 645–65. http://dx.doi.org/10.1590/s0001-37652006000400004.
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Major modifications of immune system have been observed in African trypanosomiasis. These immune reactions do not lead to protection and are also involved in immunopathology disorders. The major surface component (variable surface glycoprotein,VSG) is associated with escape to immune reactions, cytokine network dysfunctions and autoantibody production. Most of our knowledge result from experimental trypanosomiasis. Innate resistance elements have been characterised. In infected mice, VSG preferentially stimulates a Th 1-cell subset. A response of <FONT FACE=Symbol>gd</FONT> and CD8 T cells to trypanosome antigens was observed in trypanotolerant cattle. An increase in CD5 B cells, responsible for most serum IgM and production of autoantibodies has been noted in infected cattle. Macrophages play important roles in trypanosomiasis, in synergy with antibodies (phagocytosis) and by secreting various molecules (radicals, cytokines, prostaglandins,...). Trypanosomes are highly sensitive to TNF-alpha, reactive oxygen and nitrogen intermediates. TNF-alpha is also involved in cachexia. IFN-gamma acts as a parasite growth factor. These various elements contribute to immunosuppression. Trypanosomes have learnt to use immune mechanisms to its own profit. Recent data show the importance of alternative macrophage activation, including arginase induction. L-ornithine produced by host arginase is essential to parasite growth. All these data reflect the deep insight into the immune system realised by trypanosomes and might suggest interference therapeutic approaches.
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Lacy, Shannon H., Collynn F. Woeller, Thomas H. Thatcher, Krishna Rao Maddipati, Kenneth V. Honn, Patricia J. Sime, and Richard P. Phipps. "Human lung fibroblasts produce proresolving peroxisome proliferator-activated receptor-γ ligands in a cyclooxygenase-2-dependent manner." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 5 (November 1, 2016): L855—L867. http://dx.doi.org/10.1152/ajplung.00272.2016.
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Human lung fibroblasts (HLFs) act as innate immune sentinel cells that amplify the inflammatory response to injurious stimuli. Here, we use targeted lipidomics to explore the hypothesis that HLFs also play an active role in the resolution of inflammation. We detected cyclooxygenase-2 (COX-2)-dependent production of both proinflammatory and proresolving prostaglandins (PGs) in conditioned culture medium from HLFs treated with a proinflammatory stimulus, IL-1β. Among the proresolving PGs in the HLF lipidome were several known ligands for peroxisome proliferator-activated receptor-γ (PPARγ), a transcription factor whose activation in the lung yields potent anti-inflammatory, antifibrotic, and proresolving effects. Next, we used a cell-based luciferase reporter to confirm the ability of HLF supernatants to activate PPARγ, demonstrating, for the first time, that primary HLFs activated with proinflammatory IL-1β or cigarette smoke extract produce functional PPARγ ligands; this phenomenon is temporally regulated, COX-2- and lipocalin-type PGD synthase-dependent, and enhanced by arachidonic acid supplementation. Finally, we used luciferase reporter assays to show that several of the PGs in the lipidome of activated HLFs independently activate PPARγ and/or inhibit NFκB. These results indicate that HLFs, as immune sentinels, regulate both proinflammatory and proresolving responses to injurious stimuli. This novel endogenous resolution pathway represents a new therapeutic target for globally important inflammatory diseases such as chronic obstructive pulmonary disease.
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Yasmin, Shakila, Rukhsana Aziz, Muhammad Hassan, and Mehak Fatima. "TERMINATION OF PREGNANCY." Professional Medical Journal 25, no. 06 (June 10, 2018): 952–58. http://dx.doi.org/10.29309/tpmj/2018.25.06.287.
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Objectives: To compare efficacy of extra-amniotic Foley’s catheter balloon aloneversus combined use of Foley’s catheter balloon and extra-amniotic instillation of prostaglandinF2-alpha in therapeutic termination of second trimester pregnancy. Study Design: Randomizedcontrolled trial. Setting: Department of Obstetrics & Gynecology, Bahawal Victoria Hospital,Bahawalpur. Period: Two years. July 2014 to June 2016. Sample Technique: Non-probability,consecutive sampling technique. Patients & Methods: A total of 256 patients, 16 to 38 years ofage with fetal death or missed abortion on ultrasonography in 2nd trimester (14-24 gestationalweeks) of pregnancy were included in the study. Patients with previous uterine surgery, multiplepregnancies and parity>3 were excluded. Then selected patients were placed randomly intotwo groups i.e. Group A (extra-amniotic Foley’s catheter balloon alone) & Group B (Foley’scatheter balloon along with extra-amniotic instillation of prostaglandin F2-alpha), by using lotterymethod. Outcome variables like efficacy i.e. expulsion of fetus within 24 hours of induction, werenoted. Results: The mean age of women in group A was 24.51 ± 4.77 and in group B was 24.29± 4.48 years. The mean gestational age in group A was 21.65 ± 2.01 weeks and in group Bwas 21.28 ± 1.93 weeks. Efficacy was 103 (80.47%) in group A (extra-amniotic Foley’s catheterballoon alone) and 119 (92.97%) in group B (combined use of Foley’s catheter balloon andextra-amniotic instillation of prostaglandin F2-alpha) with p-value of 0.003. Conclusion: Thisstudy concluded that combined use of Foley’s catheter balloon and extra-amniotic instillationof prostaglandin F2-alpha is better and more efficacious than extra-amniotic Foley’s catheterballoon alone in therapeutic termination of second trimester pregnancy.
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Yousufzai, S. Y., and A. A. Abdel-Latif. "Effects of platelet-activating factor on the release of arachidonic acid and prostaglandins by rabbit iris smooth muscle. Inhibition by calcium channel antagonists." Biochemical Journal 228, no. 3 (June 15, 1985): 697–706. http://dx.doi.org/10.1042/bj2280697.
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Addition of physiological concentrations (10(-12)-10(-8)M) of platelet-activating factor (PAF) to rabbit iris muscle induced a rapid release (in 15s) of prostaglandin (PG)E2 and 6-oxo-PGF1 alpha, measured by radioimmunoassay and rapid release of 14C-labelled arachidonate and PGE2 in muscle prelabelled with [14C]arachidonic acid, measured by radiochromatography. These PAF actions are concentration- and time-dependent. The effect of PAF on PG release is not mediated through the cyclo-oxygenase pathway. The studies on the properties and mechanism of arachidonate release from phosphatidylinositol and other phospholipids in prelabelled irides by PAF suggest the involvement of a phospholipase A2. This conclusion is supported by the findings: (a) that both the removal of arachidonate and formation of lysophosphatidylinositol, from phosphatidylinositol, by PAF occur concomitantly in a time-dependent manner, (b) that Ca2+ is required for the agonist-induced release of arachidonate and PGE2, and (c) that in contrast to the rapid release of [3H]myo-inositol phosphates by carbachol and other Ca2+-mobilizing agonists previously reported in the iris muscle [Akhtar & Abdel-Latif (1984) Biochem. J. 224, 291-300], PAF (10(-12)-10(-8)M) did not appreciably enhance the release of [14C]myo-inositol phosphates and 32P labelling of phosphatidate and phosphatidylinositol in this tissue. Ca2+-channel antagonists, such as nifedipine, verapamil, diltiazem and manganese inhibited PAF-induced arachidonate and PGE2 release in a dose-dependent manner. K+ depolarization, which causes influx of extracellular Ca2+ in smooth muscle, did not increase the release of arachidonate and PGE2. The ability of Ca2+ antagonists to inhibit arachidonate release by PAF in this tissue probably reflects interference with PAF binding to its receptor. The PAF-induced release of arachidonate and PGE2 occur independently of the cyclo-oxygenase and lipoxygenase pathways. Whether the PAF-induced release of arachidonate and PG in the iris muscle is involved in the pathogenesis of inflammatory and/or physiological reactions in the eye, and how much the inhibitory effects of Ca2+-entry blockers on the PAF actions contribute to the therapeutic use of these drugs, remain to be established.
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Stokic, Edita, and Jela Marinkov. "Treatment of low HDL-cholesterol levels in the reduction of cardiovascular risk." Medical review 60, no. 3-4 (2007): 145–50. http://dx.doi.org/10.2298/mpns0704145s.
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Introduction. Although reduction of LDL-C levels is a priority in the treatment of dyslipidemia, not all coronary events are prevented despite aggressive LDL-C lowering, and risk reduction can be improved by treating additional lipid abnormalities. The Framingham Study was the first to demonstrate the inverse relationship between HDL-C and risk of coronary heart disease (CHD). This relationship was present at all levels of LDL-C, whereas the highest risk was associated with low HDL-C and high LDL-C. The antiatherogenic actions of HDL-cholesterol. The antiatherogenic actions of HDL-C are complex. HDL-C plays a major role in reverse cholesterol transport, mobilizing cholesterol from the periphery to the liver. In addition, cardioprotective effects of HDL-C include endothelial protection, anti-inflammatory activity, as well as antioxidant and antithrombotic effects. Treatment of low HDL cholesterol. In addition to lowering LDL-C, statins increase HDL-C by 5 to 15% by increasing apolipoprotein A-I synthesis. Fibrate therapy results in an increase in HDL-C of 10 to 25 % by activating PPAR-, which stimulates hepatic apolipoprotein A-I gene expression. Niacin is the most effective agent used for increasing HDL-C, causing increase of 15 to 35%. The side effects of niacin therapy, which is largely mediated by prostaglandins, may be minimized by the use of prolonged-release formulation of nicotinic acid. Combination therapy with HDL-raising agents, such as nicotinic acid and statin, markedly increases HDL-C, lowers LDL-C and improves the lipoproteins subclass distribution. Conclusion. New therapeutic modalities in the treatment of low HDL-C and lowering LDL-C, either in combination or as a monotherapy, may provide additional benefits in reducing CHD risk. .
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Patience, Dingom Aurelie Taylor, Keugni Armand Brice, Bendegue Emebe Alexandrie Julia, Dzeufiet Djomeni Paul Désiré, Kamtchouing Pierre, and Théophile Dimo. "Analgesic and acute inflammation properties of the aqueous extract of dried leaves of Paullinia Pinnata (Sapindaceae) Linn." International Journal of Phytomedicine 9, no. 3 (September 2, 2017): 490. http://dx.doi.org/10.5138/09750185.2115.
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<p align="left">Inflammation is frequently associated with pain. Plants continue to be major resources for therapeutic compounds against various diseases including inflammation and pain. <em>P</em><em>aullinia Pinnata </em>is used to treat several diseases, including rheumatism and abdominal pain. This study was undertaken to assess the analgesic and anti-inflammatory effects of <em>P</em><em>aullinia Pinnata. </em>The analgesic activity was evaluated by using behaviour pain model in mice. The anti-inflammatory activity was carried out by using carrageenan, dextran, histamine and serotonin induced inflammation in rat. The extract was administered orally at a dose of 200 and 400 mg/kg. The results showed that the extract significantly (P< 0.001) reduced the number of writhing induced by the acid acetic. The aqueous extract reduced significantly (P< 0.001) the paw licking time in formalin model. The effect of the extract (200mg/kg) was significantly (P< 0.001) reduced in the presence of naloxone, during the inflammatory phase. In addition, the extract significantly (P< 0.05) increase latency time at all point time and all doses on nociception induced by hot plate. Concerning inflammation induced by carrageenan and dextran, the extract significantly (P< 0.001) inhibited oedema during the experimental time at the dose of 200 mg/kg. The results suggested that<em> Paullinia pinnata</em> aqueous extract possess analgesic activities which may interfere in both peripheral and central pathway. The anti-inflammatory activities may be mediated by either inhibiting or by blocking the release of vasoactive substances like histamine, serotonin, kinins and prostaglandins. These results justify the traditional use of the plant in the treatment of pain and inflammation.</p>
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Cocnata, Christina L. "Use of Prostaglandin F2 Alpha for Cyclophosphamide-Induced Hemorrhagic Cystitis." Journal of Pharmacy Technology 10, no. 5 (September 1994): 204–6. http://dx.doi.org/10.1177/875512259401000504.
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Objective: To examine the use of prostaglandin F2 alpha in treating cyclophosphamide-induced hemorrhagic cystitis. Data Sources: An English language literature search using MEDLINE 1982–1993 and bibliographic reviews of related textbooks and review articles. Study Selection: Articles containing pertinent information regarding the therapeutic use and effects of prostaglandin F2 alpha as a treatment for cyclophosphamide-induced hemorrhagic cystitis in humans. Data Extraction: Resources were evaluated and information was extracted independently. Data Synthesis: A review of human cases suggests that intravesical administration of prostaglandin F2 alpha may be an effective bedside therapy for cyclophosphamide-induced hemorrhagic cystitis. Adverse reactions are limited primarily to local effects. The optimal dosage regimen of intravesical prostaglandin F2 alpha is not clearly established. Conclusions: Patients with intractable vesical hemorrhage secondary to cyclophosphamide administration may benefit from bedside intravesical instillation of prostaglandin F2 alpha. Information in the literature regarding prostaglandin bladder irrigation is scarce, and confined to case reports. Clinical studies are needed to endorse and/or refute the efficacy of intravesical instillation of prostaglandin F2 alpha as a treatment modality for hemorrhagic cystitis.
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Ożarowski, Marcin, Jędrzej Przystanowicz, and Artur Adamczak. "Phytochemical, pharmacological and clinical studies of petasites hybridus (l.) P. Gaertn., B. Mey. & Scherb. A review /." Herba Polonica 59, no. 4 (December 1, 2013): 108–28. http://dx.doi.org/10.2478/hepo-2013-0028.
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Abstract Preparations from rhizomes of Petasites hybridus (L.) Gaertn., B. Mey. & Scherb. (common butterbur) have a long history of use in folk medicine in treatment of several diseases as anti-inflammatory and spasmolytic drugs. Extracts from this species are of interest to researchers in the field of phytopharmacology due to their biologically active compounds, particularly two eremophilane sesquiterpenes (petasin and isopetasin), which are contained not only in rhizomes and roots, but also in leaves. Moreover, P. hybridusa contains pyrrolizidine alkaloids, which showed hepatotoxic, carcinogenic and mutagenic properties. Hence, special extracts devoid of alkaloids obtained by sub- and super-critic carbon dioxide extraction were used in the preclinical, clinical studies and phytotherapy. Our review aims to provide a literature survey of pharmacological as well as clinical trials of P. hybridus, carried out in 2000-2013. Also several studies of other species used in non-European countries have been included. Besides, the botanical description of Petasites genus and phytochemical characteristic of P. hybridus and toxicological studies of pyrrolizidine alkaloids as well as chemical profile of patented commercial extracts from rhizomes, roots and leaves of this species used in European phytotherapy have been performed. In this review, attention has also been paid to the promising and potential application of special extracts of P. hybridus not only in the prevention of migraine, treatment of allergic rhinitis symptoms, asthma and hypertension, but also in prevention and slowing the progression of neurodegenerative diseases developing with the inflammatory process in the CNS as a new therapeutic strategy. In fact, there is already an evidence of promising properties of P. hybridus extracts and sesquiterpens - decrease in the prostaglandins and leukotrienes release, inhibition of COX-1 and COX-2 activity, as well as antagonism of L-type voltage-gated calcium channels. In order to explain the new mechanisms of action of P. hybridus extracts in the CNS and their future application in phytotherapy of diseases with neuroinflammatory process, further studies should be performed.
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Baev, O. R., V. A. Gusar, A. R. Gaydarova, and I. V. Edilberg. "The use of a vaginal therapeutic system with prostaglandin for induction of labor." Meditsinskiy sovet = Medical Council, no. 16 (October 9, 2022): 84–91. http://dx.doi.org/10.21518/2079-701x-2022-16-16-84-91.
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Introduction. Induction of labor is one of the most frequent procedures in modern obstetrics, which reduces the frequency of cesarean section and improves pregnancy outcomes. However, the effectiveness and safety of labor induction methods vary. Currently, the vaginal therapeutic system (SVT) with dinoprostone is certified for use for childbirth in Russia. Aim. To conduct a review of the literature data and a pilot study of the effectiveness and safety of the vaginal therapeutic system with dinoprostone for induction of labor. Materials and methods. A review of the literature for 2001–2022 devoted to the use of vaginal systems with gradual release of prostaglandin for induction of labor was conducted. Additionally, a prospective observational study of the effectiveness and safety of the dinoprostone system was conducted in 18 pregnant women. The evaluation criteria were: the frequency of labor, the degree of maturation of the cervix on the Bishop scale, as well as the frequency of vaginal delivery. Results. Literature data indicate that SVT with dinoprostone has comparable efficacy with other methods of pre-induction / induction of labor. The system with dinoprostone has a lower frequency of the side effect of “tachysystole” than the system with misoprostol. Compared with mechanical methods, SVT is assotiated with a lower frequency of oxytocin use. The use of SVT with dinoprostone showed an efficiency of 77.8% (in terms of the of labor start or cervical ripening). No side effects requiring termination of labor induction were registered in our study. Conclusions. Thus, vaginal insertion with prostaglandin E2 – dinoprostone is an effective and safe method of pre-induction of labor. Taking into account the small sample size in our work, it is of interest to continue research in order to obtain more complete data and in comparison with other methods.
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Stridh, Sara, Fredrik Palm, and Peter Hansell. "Renal interstitial hyaluronan: functional aspects during normal and pathological conditions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 11 (June 1, 2012): R1235—R1249. http://dx.doi.org/10.1152/ajpregu.00332.2011.
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The glycosaminoglycan (GAG) hyaluronan (HA) is recognized as an important structural component of the extracellular matrix, but it also interacts with cells during embryonic development, wound healing, inflammation, and cancer; i.e., important features in normal and pathological conditions. The specific physicochemical properties of HA enable a unique hydration capacity, and in the last decade it was revealed that in the interstitium of the renal medulla, where the HA content is very high, it changes rapidly depending on the body hydration status while the HA content of the cortex remains unchanged at very low amounts. The kidney, which regulates fluid balance, uses HA dynamically for the regulation of whole body fluid homeostasis. Renomedullary HA elevation occurs in response to hydration and during dehydration the opposite occurs. The HA-induced alterations in the physicochemical characteristics of the interstitial space affects fluid flux; i.e., reabsorption. Antidiuretic hormone, nitric oxide, angiotensin II, and prostaglandins are classical hormones/compounds involved in renal fluid handling and are important regulators of HA turnover during variations in hydration status. One major producer of HA in the kidney is the renomedullary interstitial cell, which displays receptors and/or synthesis enzymes for the hormones mentioned above. During several kidney disease states, such as ischemia-reperfusion injury, tubulointerstitial inflammation, renal transplant rejection, diabetes, and kidney stone formation, HA is upregulated, which contributes to an abnormal phenotype. In these situations, cytokines and other growth factors are important stimulators. The immunosuppressant agent cyclosporine A is nephrotoxic and induces HA accumulation, which could be involved in graft rejection and edema formation. The use of hyaluronidase to reduce pathologically overexpressed levels of tissue HA is a potential therapeutic tool since diuretics are less efficient in removing water bound to HA in the interstitium. Although the majority of data describing the role of HA originate from animal and cell studies, the available data from humans demonstrate that an upregulation of HA also occurs in diabetic kidneys, in transplant-rejected kidneys, and during acute tubular necrosis. This review summarizes the current knowledge regarding interstitial HA in the role of regulating kidney function during normal and pathological conditions. It encompasses mechanistic insights into the background of the heterogeneous intrarenal distribution of HA; i.e., late nephrogenesis, its regulation during variations in hydration status, and its involvement during several pathological conditions. Changes in hyaluronan synthases, hyaluronidases, and binding receptor expression are discussed in parallel.
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Robbins, David, Thuy Le, Christopher Troung, Heather Foster, Betsy Rezner, Leah Mitchell, Lisa Guerrettaz, Pratik S. Multani, and Daniel Shoemaker. "Ex Vivo Modulation of Mobilized Peripheral Blood: Characterization of HSC and T-Cell Responses to Prostaglandin E2." Blood 124, no. 21 (December 6, 2014): 1092. http://dx.doi.org/10.1182/blood.v124.21.1092.1092.
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Abstract 16,16 dimethyl prostaglandin E2 (FT1050) was previously identified to be a critical regulator of hematopoetic stem cell (HSC) homeostasis and we hypothesized that a brief ex vivo modulation could improve patient outcomes in umbilical cord blood (UCB) transplantation by increasing the “effective dose” of HSCs. Using preclinical models, we have demonstrated that pulse treating human HSCs with FT1050 significantly enhances the homing and engraftment of donor cells to the bone marrow niche, in part by upregulating CXCR4. To date, preclinical and clinical translation of this therapeutic paradigm has focused on UCB. In an initial clinical evaluation, ex vivo modulation of UCB with FT1050 (2 hours, on site, just prior to infusion) was found to accelerate neutrophil recovery (median 17.5 vs 21 days, p = 0.045) in adult patients undergoing double UCB transplantation (Cutler, 2013). In this Phase 1b study, we also observed low rates of viral reactivation (17% incidence of CMV viremia vs. 42-67% reported in the literature) and GvHD, suggesting that FT1050 may also be having a therapeutically relevant effect on the T-cell compartment of the treated UCB units. To explore the potential therapeutic application of ex vivo modulation of other allogeneic HSC sources, we conducted a series of in vitro studies characterizing the effect of FT1050 on HSCs and T-cells derived from mobilized peripheral blood (mPB). CD34+ cells isolated from mPB or UCB were treated with 10μM FT1050 for 2 hours at 37ºC. We showed that FT1050 binds to the EP2 and EP4 receptors on the cell surface, activating adenylate cyclase which results in a rapid increase in intracellular cAMP levels. Results of a competitive antibody binding assay demonstrated robust and comparable increases in cAMP levels in CD34+ cells from both UCB and mPB. Genome-wide expression analysis of FT1050 treated CD34+ cells showed a highly similar expression response in cells isolated from mPB and UCB, including a 20-fold increase in the key HSC homing receptor CXCR4. We also observed similar FT1050-dependent increases in the surface CXCR4 protein levels and significant improvements in transwell migration rates to gradients of SDF-1. Genome-wide expression analysis within the T-cell compartments from both UCB and mPB (e.g., CD8, CD4, NK, Tregs) revealed a highly similar set of FT1050 induced genes which are involved in cell cycle (e.g., CCND1, CCNE1), tolerance (e.g., DUSP5, FLT1) and anti-viral response (e.g., CD56, EFNB2). The results of this preclinical characterization study provides the basis upon which to explore the future use of FT1050 modulated mPB in a clinical setting. Disclosures Robbins: Fate Therapeutics: Employment, Equity Ownership. Le:Fate Therapeutics: Employment, Equity Ownership. Troung:Fate Therapeutics: Employment, Equity Ownership. Foster:Fate Therapeutics: Employment, Equity Ownership. Rezner:Fate Therapeutics: Employment, Equity Ownership. Mitchell:Fate Therapeutics: Employment, Equity Ownership. Guerrettaz:Fate Therapeutics: Employment, Equity Ownership. Multani:Fate Therapeutics: Employment, Equity Ownership. Shoemaker:Fate Therapeutics: Employment, Equity Ownership.
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Owyang, Chung, and William L. Hasler. "VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 1 (July 1, 2002): G8—G15. http://dx.doi.org/10.1152/ajpgi.00095.2002.
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This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of nausea and vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias. Antral distension and increased intestinal delivery of lipids may cause slow-wave disruption and development of nausea. This may be mediated by cholinergic and serotonergic pathways. Similarly, progesterone and estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals. Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with motion sickness. This may be mediated by vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of nausea and vomiting, the search has begun for novel antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of prostaglandin synthesis inhibitors, central muscarinic receptor antagonists, and dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically implanted neurostimulator has shown promise in reducing emesis in patients with gastroparesis and gastric dysrhythmias.
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Byrne, William J. "Diagnosis and Treatment of Peptic Ulcer Disease in Children." Pediatrics In Review 7, no. 6 (December 1, 1985): 182–90. http://dx.doi.org/10.1542/pir.7.6.182.
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With advances in diagnostic technology, specifically upper gastrointestinal tract endoscopy, peptic ulcer disease in infants and children should no longer be considered rare. Whereas secondary ulcers are usually gastric and are often multiple, primary ulcers occur with almost equal frequency in the duodenum or stomach and tend to be solitary. In spite of intensive scientific investigation, the etiology of peptic ulcer disease remains unclear. Genetic factors appear to play a role and a polygenic mode of inheritance has been proposed. Emotional factors also seem to be important. Children with peptic ulcer disease tend to be of above-average intelligence, are often overachievers who have trouble dealing with frustation, and tend to internalize their feelings. Hydrochloric acid has traditionally been implicated in the pathogenesis of peptic ulcer and most therapies are directed at either "neutralizing" acid or blocking its secretion. Recently, local factors such as gastric mucus, alkaline secretion by the gastric mucosal cells, gastric blood flow, and prostaglandins have been shown to be important in local tissue resistance to acid and to digestive enzymes. The diagnosis of peptic ulcer disease depends on a high index of suspicion. Although pain is the most common symptom, there is no typical or characteristic pattern. Nausea and vomiting may also occur in conjunction with the pain. The finding of occult blood in the stool definitely warrants a diagnostic evaluation. An upper gastrointestinal tract radiographic series with small bowel follow-through should be done first. If this is nondiagnostic in a child with persistent pain or in a child with blood in the stool, upper gastrointestinal tract endoscopy is indicated. When performed by a skilled pediatric gastroenterologist, this procedure can usually be done under local sedation with minimal discomfort, either psychologic or physical, to the patient. Antacids have been the cornerstone of therapy for peptic ulcer disease and are recommended for the patient younger than 3 years of age. Cimetidine, an H2-receptor blocker, although not officially approved for use in children, is recommended for patients 3 to 12 years of age. Ranitidine, another H2 blocker, is useful in patients older than 12 years of age because of its less frequent (twice daily) dosage schedule. Sulcrafate, a coating agent, is an effective alternative to the above for the treatment of duodenal ulcer. Therapy should continue for 6 to 8 weeks. Repeat gastrointestinal series or endoscopy is only necessary if symptoms persist during therapy or return following cessation of therapy. With earlier diagnosis and newer therapeutic modalities, the long range outlook for complete recovery is good.
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Jakovljevic, Aleksandar, Emira Lazic, Neda Perunovic, and Nenad Nedeljkovic. "The use of ibuprofen in the treatment of postoperative pain in dentistry." Serbian Dental Journal 61, no. 3 (2014): 134–41. http://dx.doi.org/10.2298/sgs1403134j.
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Postoperative pain is common complication after daily dental care. Non-steroidal anti-inflammatory drugs are among most widely prescribed analgesics for management of postoperative pain. The analgesic effect of a non-steroidal antiinflammatory drug (NSAID) is related to its ability to inhibit prostaglandin synthesis. Ibuprofen (2-proprionic acid derivate) was discovered in the 1960s as a representative of NSAIDs. It is a peripherally acting analgesic with a potent anti-inflammatory action. An extensive retrospective analysis of randomized clinical trials conducted over the last 40 years demonstrated that ibuprofen is effective in moderate to severe postoperative pain for different indications in dentistry. In comparison to other NSAIDs, ibuprofen is characterized by its efficiency, safety and good tolerance. The aim of this article was to present the most important pharmacological and therapeutic characteristics and side effects of ibuprofen used for postoperative pain treatment in dentistry.
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Al Hajiri, Aufar Zimamuz Zaman, Diaz Syafrie Abdillah, and Mohammad Qoimam Bilqisthi Zulfikar. "A Prophetic Medicine: Potential Therapeutic Effect of Nigella sativa for Osteoarthritis." International Islamic Medical Journal 1, no. 2 (September 1, 2020): 68–73. http://dx.doi.org/10.33086/iimj.v1i2.1622.
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Osteoarthritis (OA) is the most common type of arthritis (inflammation of the joints). OA can affect all cartilage throughout the body, including the spine, but mainly attacks the legs from the pelvis, especially the knee to the ankle which affects about 10% of men and 18% of women over 60 years old. Pharmacotherapy, surgery, and complementary therapy are the currently managements of OA. Nigella sativa (NS) is one of the herbal plants which is part of the prophet's medicines in the Islamic world which still used. Thymoquinone (TQ) is one of NS compound, has an anti-inflammatory effect by inhibit the formation of eicosanoids in leukocytes and lipid peroxidation, or inhibit the expression of PF NF-κB subunits and p50 subunits with TNF-a promoters, and reduce levels of C-reactive protein (CRP). TQ also has a chondroprotective effects mechanism by decreases prostaglandin E2 (PGE) mediated by IL-1β and inhibits MMP synthesis in chondrocytes. Through its anti-inflammatory and chondroprotective effect, NS is a potential therapeutic agent which beneficial use for OA management without toxicological effects when given.
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Welch, KMA. "11: Naproxen Sodium in the Treatment of Migraine." Cephalalgia 6, no. 4_suppl (April 1986): 85–92. http://dx.doi.org/10.1177/03331024860060s411.
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Naproxen sodium, a potent inhibitor of prostaglandin biosynthesis and platelet aggregation, was studied for efficacy in migraine prophylaxis in a randomized, double-blind, placebo-controlled, cross-over trial. On naproxen treatment, 52% of the patients had no severe headaches whereas 19% had no severe headaches during placebo. Naproxen sodium was much better than placebo when patients' diaries were reviewed for severity of attacks, nausea, vomiting, activity reduction, duration of headache, and decreased use of therapeutic medication. Naproxen sodium can be recommended as a drug of first choice for migraine prevention.
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Sanders, L. R. "Exercise-induced acute renal failure associated with ibuprofen, hydrochlorothiazide, and triamterene." Journal of the American Society of Nephrology 5, no. 12 (June 1995): 2020–23. http://dx.doi.org/10.1681/asn.v5122020.
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Nonsteroidal anti-inflammatory drugs predispose to acute renal failure in conditions associated with decreased RBF. Such conditions include advanced age, hypertension, chronic renal insufficiency, diuretic use, and any condition decreasing effective circulating volume. Strenuous exercise also causes marked reductions in RBF. The patient discussed developed severe acute renal failure after strenuous exercise and therapeutic doses of ibuprofen and hydrochlorothiazide-triamterene. Urinalysis showed a nephritic sediment with red blood cell casts. Renal biopsy showed acute tubular necrosis and arteriolar nephrosclerosis. Although exercise-associated acute renal failure is uncommon, susceptible patients with exercise-induced renal ischemia and prostaglandin inhibition may develop this complication.
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Kirtikara, Kanyawim, Scott G. Morham, Rajendra Raghow, Stanley J. F. Laulederkind, Takuro Kanekura, Sarita Goorha, and Leslie R. Ballou. "Compensatory Prostaglandin E2 Biosynthesis in Cyclooxygenase 1 or 2 Null Cells." Journal of Experimental Medicine 187, no. 4 (February 16, 1998): 517–23. http://dx.doi.org/10.1084/jem.187.4.517.
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Prostaglandin E2 (PGE2) production in immortalized, nontransformed cells derived from wild-type, cyclooxygenase 1–deficient (COX-1−/−) or cyclooxygenase 2–deficient (COX-2−/−) mice was examined after treatment with interleukin (IL)-1β, tumor necrosis factor α, acidic fibroblast growth factor, and phorbol ester (phorbol myristate acetate). Compared with their wild-type counterparts, COX-1−/− or COX-2−/− cells exhibited substantially enhanced expression of the remaining functional COX gene. Furthermore, both basal and IL-1–induced expression of cytosolic phospholipase A2 (cPLA2), a key enzyme-regulating substrate mobilization for PGE2 biosynthesis, was also more pronounced in both COX-1−/− and COX-2−/− cells. Thus, COX-1−/− and COX-2−/− cells have the ability to coordinate the upregulation of the alternate COX isozyme as well as cPLA2 genes to overcome defects in prostaglandin biosynthetic machinery. The potential for cells to alter and thereby compensate for defects in the expression of specific genes such as COX has significant clinical implications given the central role of COX in a variety of disease processes and the widespread use of COX inhibitors as therapeutic agents.
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Smith, T. K. "The use of trichothecene-contaminated grains in feeds." Canadian Journal of Physiology and Pharmacology 68, no. 7 (July 1, 1990): 1000–1003. http://dx.doi.org/10.1139/y90-152.
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A review is presented describing the relative efficiencies of the various technologies that have been proposed to permit incorporation of mycotoxin-contaminated grains into animal diets without adversely influencing growth rate or resulting in hazardous residues in edible animal tissues. When the degree of contamination is modest, it may be possible to dilute the contaminated materials with uncontaminated grain to lower the concentration of trichothecenes below the threshold of significant biological activity. A less useful alternative to dilution is the other mechanical approach of milling to remove the most heavily contaminated fractions of the grain. Chemical destruction of trichothecenes is also a possibility. An example is the use of sodium bisulfite treatment to destroy deoxynivalenol in contaminated corn. Such treatments may, however, reduce palatability and nutritional value. When the biochemical mechanism of trichothecene toxicity is known, in vivo therapeutic treatments may be possible. It has been shown, for example, that T-2 toxin-induced changes in brain prostaglandin production can be overcome by treatment with dexamethasone resulting in increased survival. A similar effect was seen using the selective platelet activating factor antagonist BN 52021. Another approach is the use of dietary treatments to either promote in vivo detoxification of mycotoxins or to reduce absorption from the digestive tract with the aid of nonnutritive binding agents.Key words: trichothecene, Fusarium, mycotoxin, utilization, feed.
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Lim, Yun Jeong, and Hoon Jai Chun. "Recent Advances in NSAIDs-Induced Enteropathy Therapeutics: New Options, New Challenges." Gastroenterology Research and Practice 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/761060.
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The injurious effects of NSAIDs on the small intestine were not fully appreciated until the widespread use of capsule endoscopy. It is estimated that over two-thirds of regular NSAID users develop injury in the small intestinal injuries and that these injuries are more common than gastroduodenal mucosal injuries. Recently, chronic low-dose aspirin consumption was found to be associated with injury to the lower gut and to be a significant contributing factor in small bowel ulceration, hemorrhage, and strictures. The ability of aspirin and NSAIDs to inhibit the activities of cyclooxygenase (COX) contributes to the cytotoxicity of these drugs in the gastrointestinal tract. However, many studies found that, in the small intestine, COX-independent mechanisms are the main contributors to NSAID cytotoxicity. Bile and Gram-negative bacteria are important factors in the pathogenesis of NSAID enteropathy. Here, we focus on a promising strategy to prevent NSAID-induced small intestine injury. Selective COX-2 inhibitors, prostaglandin derivatives, mucoprotective drugs, phosphatidylcholine-NSAIDs, and probiotics have potential protective effects on NSAID enteropathy.