Journal articles on the topic 'Capsaicin'
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1
Bergren, D. R. "Capsaicin challenge, reflex bronchoconstriction, and local action of substance P." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 5 (May 1, 1988): R845—R852. http://dx.doi.org/10.1152/ajpregu.1988.254.5.r845.
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Capsaicin was administered as an aerosol to unanesthetized guinea pigs in a whole body plethysmograph and intravenously to anesthetized guinea pigs to investigate its mechanism of action. Capsaicin increased specific airway resistance in the unanesthetized guinea pigs and increased insufflation pressure in anesthetized guinea pigs. To investigate the possible reflex action of capsaicin, an atropine or lidocaine aerosol was administered before the capsaicin aerosol challenge in unanesthetized guinea pigs. Both lidocaine and atropine reduced the effect of capsaicin. However, neither intravenous atropine nor bilateral vagotomy antagonized the effect of injected capsaicin in the anesthetized guinea pigs. To investigate further the possible action of capsaicin, spantide (a substance P receptor antagonist) was administered before capsaicin challenge. Spantide injection in anesthetized guinea pigs attenuated the effects of the intravenous capsaicin challenge. In unanesthetized guinea pigs spantide pretreatment, as an aerosol, did not ameliorate the effects of a capsaicin aerosol challenge. However, intraperitoneal administration of spantide did reduce the effect of the capsaicin aerosol challenge as the specific airway resistance increased. Therefore, capsaicin produced its effects independent of vagal reflexes, although reflex actions of capsaicin could have occurred through other pathways. Reflex actions of capsaicin, however, were demonstrable only in the unanesthetized guinea pig. Because spantide attenuated the effect of capsaicin, increased insufflation pressure and specific airway resistance due to capsaicin challenge in both unanesthetized and anesthetized guinea pigs may be attributed, at least in part, to capsaicin's induction of substance P release or the release of other tachykinins.
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Mardhiana, Febby, Sigit Soeparjono, and Tri Handoyo. "Pengaruh Konsentrasi dan Waktu Aplikasi (NaCl) Terhadap Hasil dan Mutu Cabai Merah (Capsicum annum L.)." Agriprima, Journal of Applied Agricultural Sciences 2, no. 1 (March 24, 2018): 1–8. http://dx.doi.org/10.25047/agriprima.v2i1.81.
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Cabai (Capsicum annum L.) merupakan tanaman penting di Indonesia. Dalam 100 gram cabai segar mengandung sekitar 0,1-1,5% capsaicin yang merupakan tingkat kualitas cabai. Salah satu faktor yang mempengaruhi kadar capsaicin adalah kondisi stres salinitas. Kami mengamati efek salinitas dan waktu aplikasi pada hasil dan kandungan capsaisin. Tujuan dari penelitian ini adalah untuk mengetahui respon tanaman cabai dengan penambahan konsentrasi dan waktu aplikasi NaCl terhadap cabai dan kualitas. Penambahan konsentrasi NaCl sampai 9000 ppm dan waktu penerapan fase vegetatif NaCl dapat meningkatkan variabel kualitas kadar capsaicin dibandingkan dengan perlakuan kontrol.
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Al-Samydai, Ali, Walhan Alshaer, Emad A. S. Al-Dujaili, Hanan Azzam, and Talal Aburjai. "Preparation, Characterization, and Anticancer Effects of Capsaicin-Loaded Nanoliposomes." Nutrients 13, no. 11 (November 10, 2021): 3995. http://dx.doi.org/10.3390/nu13113995.
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Background: Medicinal plants have proven their value as a source of molecules with therapeutic potential, and recent studies have shown that capsaicin has profound anticancer effects in several types of human cancers. However, its clinical use is handicapped due to its poor pharmacokinetics. This study aims to enhance capsaicin’s pharmacokinetic properties by loading the molecule into nanoliposomes model and testing its anticancer activity. Methods: Nanoliposomes were prepared using the thin-film method, and characteristics were examined followed by qualitative and quantitative analyses of encapsulation efficiency and drug loading using HPLC at different lipid/capsaicin ratios. Cell viability assay (MTT) was used to determine IC50. Results: Capsaicin-loaded nanoliposomes showed optimum characteristics of morphology, particle size, zeta potential, and stability. In vitro anticancer activity of capsaicin and capsaicin-loaded nanoliposomes were compared against MCF7, MDA-MB-231, K562, PANC1, and A375 cell lines. Capsaicin-loaded nanoliposomes showed significant improvement in anticancer activity against cancers cell lines studied (p < 0.001), with increased selectivity against cancer cells compared to capsaicin. Conclusion: The encapsulated capsaicin nanoliposomes produced an improvement in pharmacokinetics properties, enhancing the anticancer activity and selectivity compared with capsaicin. This model seems to offer a potential for developing capsaicin formulations for the prevention and treatment of cancer.
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M, Djaldetti. "Capsaicin as a Cancer Chemopreventer- The Two Sides of the Same Coin." Gastroenterology & Hepatology International Journal 7, no. 2 (August 30, 2022): 1–13. http://dx.doi.org/10.23880/ghij-16000197.
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The pungent component of the chili pepper known as capsaicin is popular both as a spice and as a carcinopreventer. In vitro experiments and studies with animal models suggest that capsaicin may inhibit gastrointestinal, pancreatic, hepatic and other sorts of cancer development through a number of different pathways. Additionally, capsaicin may improve the therapeutic potential of traditional anti-cancer medications when taken with them. However, several reports have raised concerns that capsaicin may have a dual impact on cancer cells that promotes both cell proliferation and metastatic abilities. The purpose of this review is to examine the contradicting information regarding capsaicin’s ability to prevent cancer.
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Mizogami, Maki, and Hironori Tsuchiya. "Membrane Interactivity of Capsaicin Antagonized by Capsazepine." International Journal of Molecular Sciences 23, no. 7 (April 2, 2022): 3971. http://dx.doi.org/10.3390/ijms23073971.
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Although the pharmacological activity of capsaicin has been explained by its specific binding to transient receptor potential vanilloid type 1, the amphiphilic structure of capsaicin may enable it to act on lipid bilayers. From a mechanistic point of view, we investigated whether capsaicin and its antagonist capsazepine interact with biomimetic membranes, and how capsazepine influences the membrane effect of capsaicin. Liposomal phospholipid membranes and neuro-mimetic membranes were prepared with 1,2-dipalmitoylphosphatidylcholine and with 1-palmitoyl-2-oleoylphosphatidylcholine and sphingomyelin plus cholesterol, respectively. These membrane preparations were subjected to reactions with capsaicin and capsazepine at 0.5–250 μM, followed by measuring fluorescence polarization to determine the membrane interactivity to modify the fluidity of membranes. Both compounds acted on 1,2-dipalmitoylphosphatidylcholine bilayers and changed membrane fluidity. Capsaicin concentration-dependently interacted with neuro-mimetic membranes to increase their fluidity at low micromolar concentrations, whereas capsazepine inversely decreased the membrane fluidity. When used in combination, capsazepine inhibited the effect of capsaicin on neuro-mimetic membranes. In addition to the direct action on transmembrane ion channels, capsaicin and capsazepine share membrane interactivity, but capsazepine is likely to competitively antagonize capsaicin’s interaction with neuro-mimetic membranes at pharmacokinetically-relevant concentrations. The structure-specific membrane interactivity may be partly responsible for the analgesic effect of capsaicin.
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Kalil, Haitham, Cynthia Crichlow, and Mekki Bayachou. "Peroxynitrite Reactivity with Capsaicin: A Potential for Capsaicin-Based Sensing Devices." ECS Meeting Abstracts MA2022-02, no. 53 (October 9, 2022): 2586. http://dx.doi.org/10.1149/ma2022-02532586mtgabs.
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Peroxynitrite and other reactive oxygen species (ROS) have been linked to illnesses caused by oxidative stress, such as atherosclerosis. Accurate detection of these species in biological systems is crucial not only for understanding the etiology and course of the disease but also for creating and evaluating viable therapies. In the last 30 years, there has been an exponential increase in research into capsaicin's biological relevance. Capsaicin has analgesic, antioxidant, anti-inflammatory, anti-cancer, and anti-obesity properties. Most of these investigations have focused on the analgesic, antioxidant, and anticancer properties of this chemical compound throughout the last three decades. Capsaicin has been shown to increase the production of peroxynitrite by boosting the formation of superoxide anions in combination with nitric oxide. Preliminary UV-Vis results suggested a potential interaction at micromolar levels between capsaicin and peroxynitrite. A hyperchromic shift has been shown at a wavelength of ~ 300 nm, indicating an interaction between capsaicin and peroxynitrite, which resulted in a 2x increase in absorbance. The interaction of capsaicin and peroxynitrite was further studied using cyclic voltammetry and differential pulse voltammetry.
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Balleza-Tapia, Hugo, Pablo Dolz-Gaiton, Yuniesky Andrade-Talavera, and André Fisahn. "Capsaicin-Induced Impairment of Functional Network Dynamics in Mouse Hippocampus via a TrpV1 Receptor-Independent Pathway: Putative Involvement of Na+/K+-ATPase." Molecular Neurobiology 57, no. 2 (November 7, 2019): 1170–85. http://dx.doi.org/10.1007/s12035-019-01779-3.
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Abstract The vanilloid compound capsaicin (Cp) is best known to bind to and activate the transient receptor potential vanilloid receptor-1 (TrpV1). A growing number of studies use capsaicin as a tool to study the role of TrpV1 in the central nervous system (CNS). Although most of capsaicin’s CNS effects have been reported to be mediated by TrpV1 activation, evidence exists that capsaicin can also trigger functional changes in hippocampal activity independently of TrpV1. Recently, we have reported that capsaicin induces impairment in hippocampal gamma oscillations via a TrpV1-independent pathway. Here, we dissect the underlying mechanisms of capsaicin-induced alterations to functional network dynamics. We found that capsaicin induces a reduction in action potential (AP) firing rate and a subsequent loss of synchronicity in pyramidal cell (PC) spiking activity in hippocampus. Moreover, capsaicin induces alterations in PC spike-timing since increased first-spike latency was observed after capsaicin treatment. First-spike latency can be regulated by the voltage-dependent potassium current D (ID) or Na+/K+-ATPase. Selective inhibition of ID via low 4-AP concentration and Na+/K+-ATPase using its blocker ouabain, we found that capsaicin effects on AP spike timing were completely inhibited by ouabain but not with 4-AP. In conclusion, our study shows that capsaicin in a TrpV1-independent manner and possibly involving Na+/K+-ATPase activity can impair cognition-relevant functional network dynamics such as gamma oscillations and provides important data regarding the use of capsaicin as a tool to study TrpV1 function in the CNS.
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Rohmah, Mahya Nur, Suyadi Mitrowihardjo, and Rudi Hari Murti. "Yield, Capsaicin Content and Peroxidase Enzyme Activity of Four Chili Cultivars on Three Environments." Ilmu Pertanian (Agricultural Science) 1, no. 2 (August 17, 2017): 055. http://dx.doi.org/10.22146/ipas.11786.
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The experiment aimed to determine the effect of different environment (altitude and drought stress) on the growth, yield per plants, capsaisin levels, and peroxidase activities of four chili cultivars. Capsicum annuum (‘Lado’ and ‘Gada’) and Capsicum frutescens (‘Pelita’ and ‘Sona’) were grown with standard cultivation in medium land (± 700 m asl, Kaliurang) and low land (112 m asl, Bulaksumur) in two environments i.e. standard cultivation and drought treatment. The cultivars were arranged in Complete Randomize Design with four replications in each environment. The data were analyzed using analysis of variance with orthogonal contrast model, while the GGE biplot was applied for identification of stability. The result showed significant interaction between environment and cultivar on plant height, fruit’s weight per plant and the contents of capsaicin. Medium land of Kaliurang had suitable environment for chili cultivation of four cultivars and the high capsaicin content of C. frutescens. ‘Gada’ was significantly higher than other cultivars for fruit weight per plant in all planting conditions, while ‘Sona’ had the highest capsaicin content and was stable in all environments. Drought stress increased capsaicin content in low capsaicin content variety, in contrast to high capsaicin content cultivar. Peroxidase enzyme activity of C. frutescens was significantly higher than C. annuum, while C. annuum cultivars also shown significantly different in peroxidase activity.
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Bhutani, M., A. K. Pathak, G. Sethi, and B. B. Aggarwal. "Capsaicin induces G1/S cell cycle arrest leading to apoptosis of multiple myeloma cells through suppression of STAT3 activation and STAT3-regulated gene products." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 20039. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.20039.
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20039 Background: Agents that can block activated STAT3, a central player for proliferation, cell survival and chemoresistance, have a potential as therapeutic agents for the treatment of Multiple Myeloma (MM). Capsaicin, a spicy component of hot pepper, is a homovanillic acid derivative that preferentially induces certain cancer cells to undergo apoptosis. We have previously shown that Capsaicin blocked activation of NF-kappa B in human myeloid ML-1a cells. In this study we evaluated the effect of Capsaicin on STAT3 in MM cells. Methods: We used U266, a well-characterized MM cell line, which constitutively expresses activated STAT3. MM cells treated with Capsaicin were subjected to western blot analysis with specific antibodies to STAT3, tyrosyl phosphorylated STAT3 and STAT5. The effect of Capsaicin on nuclear-cytoplasmic compartment of STAT3 was studied by immunocytochemistry. The antiproliferative effect of Capsaicin was determined by the MTT assay and the effect on the cell cycle was determined by flowcytometry. Apoptosis of cells was measured using the Live and Dead assay. To determine the downstream targets like antiapoptotic proteins (Bcl-xL, Bcl-2, and Survivin), and cell cycle-regulators (cyclin D1) immunoblot analysis of Capsaicin treated cells was performed. Results: Capsaicin suppressed the constitutive activation of STAT3 in human MM cells in a dose- and time-dependent manner, prior to cell death. Capsaicin’s effect on STAT3 was specific as STAT5 was unaffected. Capsaicin depleted nuclear pool of STAT3 in U266 cells. Abrogation of constitutive STAT3 phosphorylation in MM cells induced G1 cell cycle arrest. The antiapoptotic proteins BCl-xl, suvivin, cyclin D1, and Bcl-2, which are encoded in target genes of STAT3, were down regulated by Capsaicin, followed by induction of apoptosis through activation of caspase-3. We further demonstrated that low dose combined Capsaicin and thalidomide/ bortezomib treatment triggered synergistic cytotoxicity. Conclusions: These findings suggest that the antitumor activity of Capsaicin is at least partially due to inhibition of STAT3 pathway and provide a basis for potential application of Capsaicin for treatment of relapsed and refractory MM. No significant financial relationships to disclose.
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Kwon, Youngjoo. "Estimation of Dietary Capsaicinoid Exposure in Korea and Assessment of Its Health Effects." Nutrients 13, no. 7 (July 19, 2021): 2461. http://dx.doi.org/10.3390/nu13072461.
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The consumption of capsaicinoids, the active components in chili peppers, has been associated with both positive and negative health effects, and the level of capsaicinoid exposure may be an important determinant. Dietary capsaicinoid exposure was estimated using a previously developed database for capsaicinoid content and a 24-h dietary recall dataset obtained from the Korea National Health and Nutrition Examination Survey. The estimated consumption level was evaluated to determine its potential effects on weight reduction and gastrointestinal distress. The estimated daily mean capsaicinoid intake was 3.25 mg (2.17 mg capsaicin), and most Koreans consumed 1–30 mg of capsaicinoids (0.67–20 mg capsaicin) in a day. No adverse effect of capsaicin consumption was reported other than abdominal pain. For long-term repeated consumption, 30 mg may be the maximum tolerable dose. However, the effects on body weight or energy balance were inconsistent in 4–12 week clinical studies conducted with various capsaicin doses (2–135 mg), which was likely due to the complex interplay between capsaicin dose, study length, and participant characteristics. Therefore, the capsaicin consumption of most Koreans was below the levels that may cause adverse effects. However, more long-term studies for the dose range of 2–20 mg are required to further characterize capsaicin’s health benefits in Koreans.
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Nassar, C. F., K. A. Barada, L. E. Abdallah, W. S. Hamdan, A. M. Taha, S. F. Atweh, and N. E. Saade. "Involvement of capsaicin-sensitive primary afferent fibers in regulation of jejunal alanine absorption." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 4 (April 1, 1995): G695—G699. http://dx.doi.org/10.1152/ajpgi.1995.268.4.g695.
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Capsaicin-sensitive primary afferent fibers (CSPA) in the small intestine regulate many functions through the release of peptides and neurotransmitters. This study was undertaken to assess the role of CSPA in the regulation of jejunal alanine absorption in the rat. In a series of in vivo experiments, the effects of the sensory neurotoxin capsaicin on small intestinal alanine absorption were evaluated. In vitro experiments were also done to study its effects on alanine uptake by isolated jejunal strips and mucosal scrapings. Jejunal alanine absorption was reduced by 27% when capsaicin (160 and 800 microM) was perfused intraluminally and by 21% when it was applied topically to the cervical vagi. On the other hand, bilateral cervical vagotomy and reversible block of vagal CSPA increased alanine absorption by 29 and 41%, respectively. In vitro, capsaicin reduced alanine uptake by intestinal strips in a dose-dependent manner. Maximal inhibition (36.5%) occurred at 400 microM with the mean ineffective concentration at 87 microM. Alanine uptake by jejunal mucosal scrapings, however, was decreased only by 6.7% when incubated with 1,600 microM capsaicin. These data suggest that vagal CSPA exerts a tonic inhibitory effect on alanine absorption and that capsaicin's inhibitory effect on alanine absorption is mediated largely by the capsaicin-sensitive afferent fibers.
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McConachie, Sean M., Ryan A. Caputo, Sheila M. Wilhelm, and Pramodini B. Kale-Pradhan. "Efficacy of Capsaicin for the Treatment of Cannabinoid Hyperemesis Syndrome: A Systematic Review." Annals of Pharmacotherapy 53, no. 11 (May 18, 2019): 1145–52. http://dx.doi.org/10.1177/1060028019852601.
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Objective: Cannabinoid hyperemesis syndrome (CHS) is characterized by cyclic vomiting, abdominal pain, and alleviation of symptoms via hot showers in chronic cannabinoid users. Capsaicin is recommended as a reasonable first-line treatment approach for CHS despite limited clinical evidence regarding its use. The objective of this study is to systematically review the efficacy data for capsaicin in CHS. Data Sources: A literature search using keywords related to cannabinoids, emesis, and capsaicin was performed in MEDLINE, CINAHL, and EMBASE from inception through March 31, 2019. Study Selection and Data Extraction: Studies and published abstracts in which capsaicin was used for CHS and clinical outcomes were reported were eligible for inclusion. Data Synthesis: A total of 241 articles were screened, of which 5 full-text articles and 6 conference abstracts were included. Full-text case reports (n = 3) and case series (n = 2) found capsaicin to be effective in a total of 18 patients. Published abstracts were in the form of case reports (n = 1), case series (n = 3), and retrospective cohort studies (n = 2). Relevance to Patient Care and Clinical Practice: Capsaicin use was described as beneficial in all case series and case reports; however, both retrospective cohort studies were unable to find a significant benefit for capsaicin on primary outcomes (emergency department length of stay). Conclusion: Current data for capsaicin efficacy in CHS is of low methodological quality. However, the limited data on alternative antiemetic therapies and capsaicin’s favorable risk-benefit profile make it a reasonable adjunctive treatment option.
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&NA;. "Capsaicin." Reactions Weekly &NA;, no. 1126 (November 2006): 8–9. http://dx.doi.org/10.2165/00128415-200611260-00021.
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Goswami, Amitabh. "Capsaicin." Journal of Pain & Palliative Care Pharmacotherapy 26, no. 4 (December 5, 2012): 373–75. http://dx.doi.org/10.3109/15360288.2012.734901.
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&NA;. "Capsaicin." Reactions Weekly &NA;, no. 1411 (July 2012): 12–13. http://dx.doi.org/10.2165/00128415-201214110-00038.
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&NA;. "Capsaicin." Reactions Weekly &NA;, no. 1249 (April 2009): 12. http://dx.doi.org/10.2165/00128415-200912490-00037.
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Prasad, B. C. N., Richa Shrivastava, and Gokare A. Ravishankar. "Capsaicin." Evidence-Based Integrative Medicine 2, no. 3 (2005): 147–66. http://dx.doi.org/10.2165/01197065-200502030-00006.
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Ochs, G., and W. Liedtke*. "Capsaicin." Aktuelle Neurologie 22, no. 04 (August 1995): 164–66. http://dx.doi.org/10.1055/s-2007-1017914.
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&NA;. "Capsaicin." Reactions Weekly &NA;, no. 1297 (April 2010): 16. http://dx.doi.org/10.2165/00128415-201012970-00047.
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&NA;. "Capsaicin." Inpharma Weekly &NA;, no. 818 (December 1991): 11. http://dx.doi.org/10.2165/00128413-199108180-00033.
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Wachtel, Ruth E. "Capsaicin." Regional Anesthesia and Pain Medicine 24, no. 4 (July 1999): 361–63. http://dx.doi.org/10.1097/00115550-199924040-00015.
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WACHTEL, R. "Capsaicin." Regional Anesthesia and Pain Medicine 24, no. 4 (July 1999): 361–63. http://dx.doi.org/10.1016/s1098-7339(99)90113-x.
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&NA;. "Capsaicin." Reactions Weekly &NA;, no. 1418 (September 2012): 17. http://dx.doi.org/10.2165/00128415-201214180-00064.
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Liu, L., M. Oortgiesen, L. Li, and S. A. Simon. "Capsaicin Inhibits Activation of Voltage-Gated Sodium Currents in Capsaicin-Sensitive Trigeminal Ganglion Neurons." Journal of Neurophysiology 85, no. 2 (February 1, 2001): 745–58. http://dx.doi.org/10.1152/jn.2001.85.2.745.
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Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, repeated exposures of capsaicin will cause desensitization to nociceptive stimuli. In cultured trigeminal ganglion (TG) neurons, we investigated mechanisms underlying capsaicin-mediated inhibition of action potentials (APs) and modulation of voltage-gated sodium channels (VGSCs). Capsaicin (1 μM) inhibited APs and VGSCs only in capsaicin-sensitive neurons. Repeated applications of capsaicin produced depolarizing potentials but failed to evoke APs. The capsaicin-induced inhibition of VGSCs was prevented by preexposing the capsaicin receptor antagonist, capsazepine (CPZ). The magnitude of the capsaicin-induced inhibition of VGSCs was dose dependent, having a K 1/2 = 0.45 μM. The magnitude of the inhibition of VGSCs was proportional to the capsaicin induced current (for – I CAP < 0.2 nA). Capsaicin inhibited activation of VGSCs without changing the voltage dependence of activation or markedly changing channel inactivation and use-dependent block. To explore the changes leading to this inhibition, it was found that capsaicin increased cAMP with a K 1/2 = 0.18 μM. At 1 μM capsaicin, this cAMP generation was inhibited 64% by10 μM CPZ, suggesting that activation of capsaicin receptors increased cAMP. The addition of 100 μM CPT-cAMP increased the capsaicin-activated currents but inhibited the VGSCs in both capsaicin-sensitive and -insensitive neurons. In summary, the inhibitory effects of capsaicin on VGSCs and the generation of APs are mediated by activation of capsaicin receptors. The capsaicin-induced activation of second messengers, such as cAMP, play a part in this modulation. These data distinguish two pathways by which neuronal sensitivity can be diminished by capsaicin: by modulation of the capsaicin receptor sensitivity, since the block of VGSCs is proportional to the magnitude of the capsaicin-evoked currents, and by modulation of VGSCs through second messengers elevated by capsaicin receptor activation. These mechanisms are likely to be important in understanding the analgesic effects of capsaicin.
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Barada, K. A., S. S. Dika, S. F. Atweh, N. E. Saade, and C. F. Nassar. "Acute and neonatal capsaicin treatment inhibit jejunal amino acid absorption through a Na+-dependent mechanism." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 4 (April 1, 1997): G815—G821. http://dx.doi.org/10.1152/ajpgi.1997.272.4.g815.
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It has recently been shown that capsaicin inhibits alanine absorption in rat jejunum via mechanisms that involve intestinal capsaicin-sensitive primary afferent (CSPA) fibers. This study provides further evidence that the effect of capsaicin is neurally mediated and demonstrates that CSPA fibers regulate Na+-dependent amino acid absorption. In vivo, basal alanine absorption in rats neonatally treated with capsaicin was reduced by 35% below control. Furthermore, intraluminal perfusion of 400 microM capsaicin reduced jejunal alanine absorption by 31% in sham rats but had no significant effect in rats neonatally treated with capsaicin. In vitro, capsaicin significantly reduced uptake of alanine and proline by jejunal strips but had no effect on uptake of lysine. Tetrodotoxin (0.2 microM) partially blocked the effects of capsaicin but did not itself affect alanine absorption. Capsaicin reduced unidirectional mucosal-to-serosal alanine (1 mM) influx by 33%, an effect that becomes significant after 5 min of preincubation with capsaicin. Neonatal capsaicin treatment reduced basal alanine influx in jejunal strips by 37%; however, preincubation of these strips with capsaicin had no significant effect. Kinetic analysis of alanine steady-state uptake and influx by jejunal strips incubated with capsaicin revealed that capsaicin reduced the Na+-dependent component of alanine influx into intestinal epithelial cells. Long-term sensory denervation by capsaicin also decreased the Na+-dependent component of alanine absorption. These data suggest that intestinal capsaicin-sensitive primary afferent fibers regulate Na+-dependent amino acid absorption.
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Tamura, C. S., and R. C. Ritter. "Intestinal capsaicin transiently attenuates suppression of sham feeding by oleate." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 2 (August 1, 1994): R561—R568. http://dx.doi.org/10.1152/ajpregu.1994.267.2.r561.
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Intraintestinal infusion of oleic acid reduces food intake in rats and other mammals. The neural mechanisms that mediate this behavioral response to intestinal stimulation are incompletely appreciated. We have found that intraintestinal infusion of capsaicin reduces sham feeding. In addition, 24 h after a single intestinal capsaicin infusion, reduction of sham feeding by intestinal oleate infusion was attenuated. However, by 48 h post-capsaicin, suppression of sham feeding by oleate had returned to pre-capsaicin levels. Repeated intestinal administration of capsaicin produced less attenuation of oleate-induced suppression of sham feeding, suggesting the development of tolerance to capsaicin. Unlike systemic capsaicin, intestinal capsaicin does not impair cholecystokinin-induced reduction of feeding or the corneal chemosensory reflex. Furthermore, there are no histochemical signs of vagal sensory degeneration in the hindbrain after intraintestinal capsaicin. Our results suggest that a capsaicin-sensitive substrate in or near the intestine is responsible for mediating the reduction of sham feeding by intestinal oleate infusion.
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Rains, Chris, and Harriet M. Bryson. "Topical Capsaicin." Drugs & Aging 7, no. 4 (October 1995): 317–28. http://dx.doi.org/10.2165/00002512-199507040-00007.
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&NA;. "Capsaicin interaction." Reactions Weekly &NA;, no. 334 (January 1991): 4. http://dx.doi.org/10.2165/00128415-199103340-00014.
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Mao, Sally Wen. "Capsaicin Eclogue." Colorado Review 40, no. 1 (2013): 149. http://dx.doi.org/10.1353/col.2013.0011.
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&NA;. "Intranasal capsaicin." Inpharma Weekly &NA;, no. 811 (November 1991): 15. http://dx.doi.org/10.2165/00128413-199108110-00037.
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Vorndam, Paul E. "Capsaicin Hazard." Journal of Chemical Education 77, no. 4 (April 2000): 444. http://dx.doi.org/10.1021/ed077p444.1.
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Kumar, Thriveni Vasanth, Manjunatha H., and Rajesh Kp. "ANTI-INFLAMMATORY ACTIVITY OF CURCUMIN AND CAPSAICIN AUGMENTED IN COMBINATION." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 6 (June 1, 2017): 145. http://dx.doi.org/10.22159/ijpps.2017v9i6.18635.
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Objective: Dietary curcumin and capsaicin are well known for their health beneficial potencies. The current study was done to assess the anti-inflammatory activity of curcumin, capsaicin and their combination by employing in vitro and in vivo models.Methods: We investigated the protective effect of curcumin, capsaicin and their combination using in vitro heat induced human red blood cell (HRBC) membrane stabilisation, in vivo 3% agar induced leukocyte mobilisation and acetic acid induced vascular permeability assay.Results: Curcumin, capsaicin and their combination exhibited concentration dependent protective effect against heat-induced HRBC membrane destabilisation, while combined curcumin and capsaicin restored 87.0±0.64 % membrane stability and it is found to be better than curcumin, capsaicin and diclofenac sodium (75.0±0.25. 72±0.9 and 80.0±0.31 %) protective effect. In agar suspension induced leukocyte mobilization assay, the combined curcumin and capsaicin had shown 39.5±1.58 % of inhibition compared to individual curcumin and capsaicin, which showed moderate inhibition of 16.0±3.14 and 21.6±2.17 % respectively. Besides, the combined curcumin and capsaicin had shown highly significant inhibition of acetic acid-induced vascular permeability in rats (62.0±3.14 %), whereas individual curcumin and capsaicin showed moderate inhibition of vascular permeability with 36.0±2.41 and 43.0±1.92 % respectively.Conclusion: This study demonstrates the significant anti-inflammatory property of combined curcumin and capsaicin at half of the individual concentration of curcumin and capsaicin.
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Pasierski, Michał, and Bartłomiej Szulczyk. "Beneficial Effects of Capsaicin in Disorders of the Central Nervous System." Molecules 27, no. 8 (April 12, 2022): 2484. http://dx.doi.org/10.3390/molecules27082484.
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Capsaicin is a natural compound found in chili peppers and is used in the diet of many countries. The important mechanism of action of capsaicin is its influence on TRPV1 channels in nociceptive sensory neurons. Furthermore, the beneficial effects of capsaicin in cardiovascular and oncological disorders have been described. Many recent publications show the positive effects of capsaicin in animal models of brain disorders. In Alzheimer’s disease, capsaicin reduces neurodegeneration and memory impairment. The beneficial effects of capsaicin in Parkinson’s disease and depression have also been described. It has been found that capsaicin reduces the area of infarction and improves neurological outcomes in animal models of stroke. However, both proepileptic and antiepileptic effects of capsaicin in animal models of epilepsy have been proposed. These contradictory results may be caused by the fact that capsaicin influences not only TRPV1 channels but also different molecular targets such as voltage-gated sodium channels. Human studies show that capsaicin may be helpful in treating stroke complications such as dysphagia. Additionally, this compound exerts pain-relieving effects in migraine and cluster headaches. The purpose of this review is to discuss the mechanisms of the beneficial effects of capsaicin in disorders of the central nervous system.
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Zhu, Feng-Xia, Xiang-Yang Zhang, Michal A. Olszewski, and N. Edward Robinson. "Mechanism of capsaicin-induced relaxation in equine tracheal smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 5 (November 1, 1997): L997—L1001. http://dx.doi.org/10.1152/ajplung.1997.273.5.l997.
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The effects of capsaicin and neuropeptides were examined in equine tracheal smooth muscle (TSM). Neither capsaicin nor substance P (SP) contracted TSM. Capsaicin (100 μM) elicited relaxation in TSM contracted with methacholine. This relaxation was not mimicked by SP or calcitonin gene-related peptide (CGRP). Relaxation was not attenuated by removal of the epithelium or by pretreatment of tissue with meclofenamate or the nitric oxide (NO) synthase inhibitor N G-nitro-l-arginine. Previous exposure of TSM to capsaicin did not eliminate the relaxation responses to subsequent capsaicin. Although vasoactive intestinal peptide (VIP) elicited marked relaxation that was attenuated by α-chymotrypsin, α-chymotrypsin did not affect the capsaicin-induced relaxation. Capsaicin-induced relaxation was abolished by charybdotoxin, a blocker of large-conductance Ca2+-activated K+ channels. These results indicate that capsaicin-induced equine TSM relaxation is not mediated either by neuropeptides such as SP or CGRP released from capsaicin-sensitive sensory nerves or by prostanoids, NO, or VIP. Relaxation is due to the effect of capsaicin on large-conductance Ca2+-activated K+ channels. The peptidergic nerves play no important role in the regulation of TSM tone in horse airways.
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Vanner, S., and W. K. MacNaughton. "Capsaicin-sensitive afferent nerves activate submucosal secretomotor neurons in guinea pig ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 2 (August 1, 1995): G203—G209. http://dx.doi.org/10.1152/ajpgi.1995.269.2.g203.
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This study examined whether capsaicin-sensitive sensory nerves regulate intestinal ion transport using both Ussing chamber and intracellular recording techniques in in vitro submucosal preparations from the guinea pig ileum. In Ussing chamber studies, serosal application of capsaicin (20 nM-20 microM) evoked a biphasic dose-dependent increase in short-circuit current (Isc) (maximal effective concentration 200 nM and 2 microM, respectively). In chloride-free buffer, capsaicin responses were significantly reduced. Capsaicin evoked little or no response when extrinsic sensory nerve fibers had been surgically removed and tetrodotoxin and low-calcium and high-magnesium solutions blocked responses to capsaicin. In epithelial preparations devoid of submucosal neurons, capsaicin had virtually no effect, suggesting that responses evoked by capsaicin-sensitive nerves result from activation of submucosal secretomotor neurons. Intracellular recordings from single submucosal neurons demonstrated that superfusion with capsaicin (2 microM) depolarized neurons with an associated decreased conductance. Depolarizations were completely desensitized when capsaicin was reapplied, but synaptic inputs were unaffected. This study suggests that capsaicin-sensitive nerves can regulate ion transport in the gastrointestinal tract by release of neurotransmitter(s) that activate submucosal secretomotor neurons.
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Malewicz, Nathalie M., Zahra Rattray, Sebastian Oeck, Sebastian Jung, Vicente Escamilla-Rivera, Zeming Chen, Xiangjun Tang, Jiangbing Zhou, and Robert H. LaMotte. "Topical Capsaicin in Poly(lactic-co-glycolic)acid (PLGA) Nanoparticles Decreases Acute Itch and Heat Pain." International Journal of Molecular Sciences 23, no. 9 (May 9, 2022): 5275. http://dx.doi.org/10.3390/ijms23095275.
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Background: Capsaicin, the hot pepper agent, produces burning followed by desensitization. To treat localized itch or pain with minimal burning, low capsaicin concentrations can be repeatedly applied. We hypothesized that alternatively controlled release of capsaicin from poly(lactic-co-glycolic acid) (PLGA) nanoparticles desensitizes superficially terminating nociceptors, reducing burning. Methods: Capsaicin-loaded PLGA nanoparticles were prepared (single-emulsion solvent evaporation) and characterized (size, morphology, capsaicin loading, encapsulation efficiency, in vitro release profile). Capsaicin-PLGA nanoparticles were applied to murine skin and evaluated in healthy human participants (n = 21) for 4 days under blinded conditions, and itch and nociceptive sensations evoked by mechanical, heat stimuli and pruritogens cowhage, β-alanine, BAM8-22 and histamine were evaluated. Results: Nanoparticles (loading: 58 µg capsaicin/mg) released in vitro 23% capsaicin within the first hour and had complete release at 72 h. In mice, 24 h post-application Capsaicin-PLGA nanoparticles penetrated the dermis and led to decreased nociceptive behavioral responses to heat and mechanical stimulation (desensitization). Application in humans produced a weak to moderate burning, dissipating after 3 h. A loss of heat pain up to 2 weeks was observed. After capsaicin nanoparticles, itch and nociceptive sensations were reduced in response to pruritogens cowhage, β-alanine or BAM8-22, but were normal to histamine. Conclusions: Capsaicin nanoparticles could be useful in reducing pain and itch associated with pruritic diseases that are histamine-independent.
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Sharma, Neha, Huong T. T. Phan, Tsuyoshi Yoda, Naofumi Shimokawa, Mun’delanji C. Vestergaard, and Masahiro Takagi. "Effects of Capsaicin on Biomimetic Membranes." Biomimetics 4, no. 1 (February 13, 2019): 17. http://dx.doi.org/10.3390/biomimetics4010017.
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Capsaicin is a natural compound that produces a warm sensation and is known for its remarkable medicinal properties. Understanding the interaction between capsaicin with lipid membranes is essential to clarify the molecular mechanisms behind its pharmacological and biological effects. In this study, we investigated the effect of capsaicin on thermoresponsiveness, fluidity, and phase separation of liposomal membranes. Liposomal membranes are a bioinspired technology that can be exploited to understand biological mechanisms. We have shown that by increasing thermo-induced membrane excess area, capsaicin promoted membrane fluctuation. The effect of capsaicin on membrane fluidity was dependent on lipid composition. Capsaicin increased fluidity of (1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) membranes, while it rigidified DOPC and cholesterol-based liposomes. In addition, capsaicin tended to decrease phase separation of heterogeneous liposomes, inducing homogeneity. We imagine this lipid re-organization to be associated with the physiological warming sensation upon consumption of capsaicin. Since capsaicin has been reported to have biological properties such as antimicrobial and as antiplatelet, the results will help unravel these biological properties.
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Watanabe, T., T. Kawada, M. Kurosawa, A. Sato, and K. Iwai. "Adrenal sympathetic efferent nerve and catecholamine secretion excitation caused by capsaicin in rats." American Journal of Physiology-Endocrinology and Metabolism 255, no. 1 (July 1, 1988): E23—E27. http://dx.doi.org/10.1152/ajpendo.1988.255.1.e23.
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Capsaicin enhances adrenal medullary catecholamine secretion. The participation of the central nervous system on this enhancement by capsaicin was investigated in alpha-chloralose-urethan- or halothane-anesthetized rats. Intravenous administration of capsaicin caused a rapid and marked increase in adrenal sympathetic nerve activity. The nerve activity began to show an increase with the administration of capsaicin at a dosage of 20 micrograms/kg and significantly increased with a dosage of 200 micrograms/kg, i.e., capsaicin was found to cause a dose-dependent increase in adrenal nerve activity. Cholinergic blocking with hexamethonium bromide and atropine sulfate (1 and 5 mg/kg iv, respectively) attenuated the adrenal epinephrine secretion caused by capsaicin. The direct action of capsaicin on adrenal catecholamine secretion was examined using a retrograde perfusion system of left adrenal gland. Up to 8.2 X 10(-5) M capsaicin did not enhance catecholamine secretion from the adrenal gland. These results suggest that the enhancement of physiological catecholamine secretion by capsaicin is mainly through activation of the central nervous system.
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Jiang, Rui, Fang Zhang, Zhu Ping Yin, and Shen Zhou Lu. "In Vitro Controlled Release of Topically Applied Capsaicin from Silk Hydrogel: A Study Contributed to the Pain Relief System." Materials Science Forum 815 (March 2015): 332–35. http://dx.doi.org/10.4028/www.scientific.net/msf.815.332.
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The availability of a safety and efficient vehicle for pain relief system remains major challenge. The clinical applications of capsaicin are restricted by lacking a long-term drug delivery system The purpose of the present study is to control the release of topically applied capsaicin from silk fibroin hydrogel, all factors including proportions of silk fibroin, amount of capsaicin and penetration enhancer are studied. The capsaicin release behavior was measured by using x-ray fluorescence spectroscopy (XRF). X-ray diffraction (XRD) was used to investigate structure of the silk fibroin hydrogels. The results indicate that the silk can protect the capsaicin and also all factors involved influence the capsaicin release behavior. The release of the capsaicin may be controlled exactly by changing the factors involved. So the silk fibroin hydrogels make the capsaicin a promising pain relief drug used in clinic in the future.
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Dai, Zijian, Siqi Li, Yantong Meng, Qingyu Zhao, Yiyun Zhang, Zhuoma Suonan, Yuge Sun, Qun Shen, Xiaojun Liao, and Yong Xue. "Capsaicin Ameliorates High-Fat Diet-Induced Atherosclerosis in ApoE−/− Mice via Remodeling Gut Microbiota." Nutrients 14, no. 20 (October 17, 2022): 4334. http://dx.doi.org/10.3390/nu14204334.
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Capsaicin is a pungent alkaloid abundantly present in peppers with outstanding biological activities, including the anti-atherosclerosis effect. Previous studies revealed that gut microbiota played an important role in the beneficial effects of capsaicin, but whether it is essential for the anti-atherosclerosis effect of capsaicin is unclear. This study evaluated the anti-atherosclerosis effect of capsaicin in ApoE−/− mice and further explored the role of depleting gut microbiota in the improvement of atherosclerosis. The results showed that capsaicin administration could prevent the development of atherosclerosis and improve serum lipids and inflammation, while antibiotic intervention abolished the alleviation of atherosclerosis by capsaicin. In addition, capsaicin administration could significantly increase the abundance of Turicibacter, Odoribacter, and Ileibacterium in feces, and decrease the abundance of deoxycholic acid, cholic acid, hypoxanthine, and stercobilin in cecal content. Our study provides evidence that gut microbiota plays a critical role in the anti-atherosclerosis effect of capsaicin.
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Giri, Tapan Kumar, Payel Roy, and Subhasis Maity. "Formulation and Characterization of Solid Dispersion Containing Capsaicin for the Treatment of Diabetes." Current Drug Therapy 15, no. 3 (October 14, 2020): 219–25. http://dx.doi.org/10.2174/1574885514666190916152432.
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Background: Chili peppers are widely used in many cuisines as a spice, and capsaicin is the main component. It has been reported that capsaicin acts as an antihyperglycemic agent. However, it shows poor aqueous solubility and bioavailability. Objective: The is to enhance the aqueous solubility and antihyperglycemic activity of capsaicin through solid dispersion formulation. Methods: Solid dispersions were prepared by the solvent evaporation method using polyethylene glycol 6000 (PEG 6000) as a hydrophilic carrier. Polymer-drug miscibility and drug crystallinity were characterized through the differential thermal analysis and X-ray powder patterns analysis. Solid dispersions were evaluated for solubility, in vitro drug dissolution and in vivo animal study in rats. Results: Results of x-ray powder patterns analysis showed a considerable reduction of drug crystallinity in solid dispersion. Differential thermal analysis result revealed a complete disappearance of capsaicin melting onset temperature in solid dispersion. From the phase solubility data, it was observed that the aqueous solubility of capsaicin was increased with increasing concentration of PEG 6000. Solid dispersion formulation showed considerable enhancement of in vitro release of drugs in comparison to pure capsaicin. In vivo animal study in rats shows that the solid dispersion containing capsaicin significantly reduced the blood glucose level in comparison to the free capsaicin. Conclusion: Higher anti-hyperglycemic effect of capsaicin loaded solid dispersion in comparison to the pure drug may be due to the enhancement of aqueous solubility of capsaicin. Thus, the solid dispersion of capsaicin showed a simple approach for capsaicin delivery with improved antidiabetic activity.
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Shibata, Mamoru, Yohei Kayama, Tsubasa Takizawa, Keiji Ibata, Toshihiko Shimizu, Michisuke Yuzaki, Norihiro Suzuki, and Jin Nakahara. "Resilience to capsaicin-induced mitochondrial damage in trigeminal ganglion neurons." Molecular Pain 16 (January 2020): 174480692096085. http://dx.doi.org/10.1177/1744806920960856.
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Capsaicin is an agonist of transient receptor potential cation channel subfamily V member 1 (TRPV1). Strong TRPV1 stimulation with capsaicin causes mitochondrial damage in primary sensory neurons. However, the effect of repetitive and moderate exposure to capsaicin on the integrity of neuronal mitochondria remains largely unknown. Our electron microscopic analysis revealed that repetitive stimulation of the facial skin of mice with 10 mM capsaicin induced short-term damage to the mitochondria in small-sized trigeminal ganglion neurons. Further, capsaicin-treated mice exhibited decreased sensitivity to noxious heat stimulation, indicating TRPV1 dysfunction, in parallel with the mitochondrial damage in the trigeminal ganglion neurons. To analyze the capsaicin-induced mitochondrial damage and its relevant cellular events in detail, we performed cell-based assays using TRPV1-expressing PC12 cells. Dose-dependent capsaicin-mediated mitochondrial toxicity was observed. High doses of capsaicin caused rapid destruction of mitochondrial internal structure, while low doses induced mitochondrial swelling. Further, capsaicin induced a dose-dependent loss of mitochondria and autophagy-mediated degradation of mitochondria (mitophagy). Concomitantly, transcriptional upregulation of mitochondrial proteins, cytochrome c oxidase subunit IV, Mic60/Mitofilin, and voltage-dependent anion channel 1 was observed, which implied induction of mitochondrial biogenesis to compensate for the loss of mitochondria. Collectively, although trigeminal ganglion neurons transiently exhibit mitochondrial damage and TRPV1 dysfunction following moderate capsaicin exposure, they appear to be resilient to such a challenge. Our in vitro data show a dose–response relationship in capsaicin-mediated mitochondrial toxicity. We postulate that induction of mitophagy and mitochondrial biogenesis in response to capsaicin stimulation play important roles in repairing the damaged mitochondrial system.
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Sánchez, Belén G., Alicia Bort, José M. Mora-Rodríguez, and Inés Díaz-Laviada. "The Natural Chemotherapeutic Capsaicin Activates AMPK through LKB1 Kinase and TRPV1 Receptors in Prostate Cancer Cells." Pharmaceutics 14, no. 2 (January 29, 2022): 329. http://dx.doi.org/10.3390/pharmaceutics14020329.
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The natural bioactive compound capsaicin has been reported to have anticancer activity, although the underlying mechanism of action has not been completely clarified. Herein, we investigated the mechanism whereby capsaicin exerts antitumor effects on prostate cancer cells. We found that capsaicin activated AMP-activated kinase (AMPK) and promoted cell death in the LKB1-expressing prostate cancer cell lines LNCaP and PC3, but not in the liver kinase B1 (LKB1)-null cell line DU-145. Capsaicin treatment stimulated LKB1 phosphorylation and activated AMPK in LKB1-expressing cells. In addition, LKB1 silencing in LNCaP and PC3 cells abrogated capsaicin-induced AMPK activation, while the overexpression of LKB1 by lentiviral infection in DU-145 cells induced capsaicin-triggered AMPK phosphorylation. Moreover, the calcium/calmodulin-dependent kinase kinase 2 (CaMKK2) inhibitor STO-609 did not modify the activation of AMPK induced by capsaicin, suggesting a CaMKK2-independent mechanism. Capsaicin-induced LKB1 phosphorylation was dependent on the transient receptor potential cation channel subfamily V member 1 (TRPV1), since TRPV1 knocked down by shRNA abolished LKB1 and AMPK phosphorylation in LKB1-expressing cells. Altogether, our results showed that capsaicin affected AMPK activity in an LKB1- and TRPV1-dependent fashion, linking TRPV1 with cell fate. These data also suggest that capsaicin may be a rational chemotherapeutic option for prostate tumors.
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Holzer, P., E. H. Livingston, A. Saria, and P. H. Guth. "Sensory neurons mediate protective vasodilatation in rat gastric mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 3 (March 1, 1991): G363—G370. http://dx.doi.org/10.1152/ajpgi.1991.260.3.g363.
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Sensory nerve stimulation by intragastric capsaicin (160 microM) prevents ethanol injury to the gastric mucosa and facilitates gastric mucosal blood flow (GMBF). The present study examined whether the capsaicin-induced increase in GMBF accounts for mucosal protection. Gastric perfusion of capsaicin (160 microM) in urethan-anesthetized rats did not change blood pressure but significantly enhanced GMBF as measured by hydrogen gas clearance. The same increase in GMBF was seen when capsaicin was administered together with an injurious concentration of ethanol (25%). GMBF was facilitated by capsaicin in a dose-related manner (10-640 microM), and the dose-dependent vasodilatation was significantly correlated with a dose-dependent reduction of gross damage to the mucosa. Histology showed that capsaicin prevented deep but not superficial mucosal damage. The vasodilator and protective effects of capsaicin resulted from stimulation of sensory neurons and propagation of nerve activity, since they were blocked after ablation of capsaicin-sensitive neurons or local intra-arterial infusion of tetrodotoxin. This and the finding of a limited access of intragastric capsaicin to the gastric wall indicates that the vasodilator and protective effects of capsaicin are mediated by a neural reflex. It is concluded that facilitation of GMBF is the major mechanism of sensory nerve-mediated prevention of gastric mucosal injury.
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White, C. B., A. M. Roberts, and I. G. Joshua. "Arteriolar dilation mediated by capsaicin and calcitonin gene-related peptide in rats." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1411—H1415. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1411.
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In addition to altering vascular tone by stimulating primary afferent nerves and acting through reflex pathways, capsaicin acts locally. We examined effects of topically applied capsaicin on arteriolar diameter in striated muscle and tested the hypothesis that capsaicin can alter microvascular tone by releasing substance P (SP) or calcitonin gene-related peptide (CGRP). In anesthetized rats, the right cremaster muscle was exposed and suspended in a tissue bath filled with a physiological salt solution. Diameters of third-order arterioles were displayed and measured using in vivo video microscopy. In 17 of 20 rats, addition of capsaicin (3 x 10(-7) M) to the bath dilated arterioles (85 +/- 14% above control). Failure of a second administration of capsaicin to produce a sustained dilation in 6 of 7 arterioles that had previously dilated to capsaicin is consistent with the hypothesis that this agent causes depletion of an endogenous vasodilator. Pretreatment with an SP inhibitor did not alter capsaicin-induced dilation. CGRP (1 x 10(-10) to 2 x 10(-8) M) caused dilation similar to that caused by capsaicin. Pretreatment with a CGRP inhibitor to the bath prevented capsaicin-induced dilation, but not constriction. These results suggest that capsaicin can dilate microvessels by releasing CGRP, which can modulate tone.
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Mizoguchi, H., and M. L. Bergeron. "Effect of capsaicin on nasal secretion in anesthetized ferrets." Journal of Applied Physiology 70, no. 1 (January 1, 1991): 282–86. http://dx.doi.org/10.1152/jappl.1991.70.1.282.
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In urethan-anesthetized ferrets, we investigated the nasal response to capsaicin infused via a catheter inserted retrogradely into the lingual artery. Capsaicin dose-dependently increased fluid output from the nose (nasal fluid output) and the lateral nasal gland (glandular fluid output). The secretory response to capsaicin (80 nmol/kg ia) was completely blocked by atropine and hexamethonium, indicating that a cholinergic reflex mediates capsaicin-induced nasal hypersecretion in this model. The amount of nasal secretions collected as nasal fluid output was similar to that collected as glandular fluid output, indicating that the lateral nasal gland contributes significantly to this increase in nasal secretions induced by intra-arterially administered capsaicin. In addition, the nasal fluid output had a higher protein concentration and osmolality than the glandular fluid output. This finding suggests that the gland is not the sole site of action of capsaicin on the nasal secretory response. It is likely that capsaicin also increases microvascular permeability, thereby contributing further to the alteration in the nasal secretions. Finally, repeated subcutaneous injections of capsaicin significantly reduced the secretory response to capsaicin, indicating the development of desensitization in vivo. These results support the role of capsaicin-sensitive sensory nerves in mediating a secretory response in the ferret nose.
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Liu, L., and S. A. Simon. "Modulation of I A Currents by Capsaicin in Rat Trigeminal Ganglion Neurons." Journal of Neurophysiology 89, no. 3 (March 1, 2003): 1387–401. http://dx.doi.org/10.1152/jn.00210.2002.
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When capsaicin, the pungent compound in hot pepper, is applied to epithelia it produces pain, allodynia, and hyperalgesia. We investigated, using whole cell path clamp, whether some of these responses induced by capsaicin could be a consequence of capsaicin blocking I Acurrents, a reduction in which, such as occurs in injury, increases neuronal excitability. In capsaicin-sensitive (CS) rat trigeminal ganglion (TG) neurons, capsaicin inhibited I A currents in a dose-dependent manner. I A currents were reduced 49% by 1 μM capsaicin. In capsaicin-insensitive (CIS) rat TG neurons, or small-diameter mouse VR1−/− neurons, 1 μM capsaicin inhibited I A currents 9 and 3%, respectively. These data suggest that in CS neurons the vast majority of the capsaicin-induced inhibition of I Acurrents occurs as a consequence of the activation of vanilloid receptors. Capsaicin (1 μM) did not alter the I A conductance-voltage relationship but shifted the inactivation-voltage curve about 15 mV to hyperpolarizing voltages, thereby increasing the number of inactivated I A channels at the resting potential. I A currents were relatively unaffected by 1 mM CTP-cAMP or 500 nM phorbol-12, 13-dibuterate (a protein kinase C agonist) but were inhibited by 20–30% with either 1 mM CTP-cGMP or 25 μM N-(6-aminohexyl)-5-chloro-1-napthalenesulfonamide HCl (a calcium-calmodulin kinase inhibitor). In the presence of 0.5 μM KT5823, an inhibitor of protein kinase G (PKG) pathways, 1 μM capsaicin inhibited I A by only 26%. In summary, in CS neurons, capsaicin decreases I A currents through the activation of vanilloid receptors. That activation, partially through the activation of cGMP-PKG and calmodulin-dependent pathways should result in increased excitability of capsaicin-sensitive nociceptors.
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Kandagalla, Shivananda, Sharath Belenahalli Shekarappa, Gollapalli Pavan, Umme Hani, and Manjunatha Hanumanthappa. "Exploring the Potential of Capsaicin Against Cancer Metastasis Based on TGF-β Signaling Modulation Through Module-based Network Pharmacology Approach." Current Drug Discovery Technologies 17, no. 5 (December 23, 2020): 647–60. http://dx.doi.org/10.2174/1570163816666190515104041.
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Background: Capsaicin is an active alkaloid /principal component of red pepper responsible for the pungency of chili pepper. Capsaicin by changing the intracellular redox homeostasis regulate a variety of signaling pathways ultimately producing a divergent cellular outcome. Several reports showed the potential of capsaicin against cancer metastasis, however unexplored molecular mechanism is still an active part of the research. Several growth factors have a critical role during cancer metastasis among them TGF- β signaling play a vital role. Methods: The present study aimed at analyzing capsaicin modulation of TGF-β signaling using network pharmacology approach. The chemical and protein interaction data of capsaicin was curated and abstracted using STITCH4.0, PubChem and ChEMBL database. Further, the compiled data set was subjected to the pathway and functional enrichment analysis using Protein Analysis THrough Evolutionary Relationship (PANTHER) and, Database for Annotation, Visualization, and Integrated Discovery (DAVID) database. Meanwhile, the pattern of amino acid composition across the capsaicin targets was analyzed using the EMBOSS Pepstat tool. Capsaicin targets involved in TGF- β were identified and their Protein-Protein Interaction (PPI) network constructed using STRING v10 and Cytoscape (v 3.2.1). From the above-constructed network, the clusters were mined using the MCODE clustering algorithm and finally binding affinity of capsaicin with its targets involved in TGF-β signaling pathway was analyzed using Autodock Vina. Results: The analysis explored capsaicin targets and, their associated functional and pathway annotations. Besides, the analysis also provides a detailed distinct pattern of amino acid composition across the capsaicin targets. The capsaicin targets described as MAPK14, JUN, SMAD3, MAPK3, MAPK1 and MYC involved in TGF-β signaling pathway through pathway enrichment analysis. The binding mode analysis of capsaicin with its targets has shown high affinity with MAPK3, MAPK1, JUN and MYC. Conclusion: The study explores the potential of capsaicin as a potent modulator of TGF-β signaling pathway during cancer metastasis and proposes new methodology and mechanism of action of capsaicin against TGF- β signaling pathway.
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Renate, Dharia, Filli Pratama, Kiki Yuliati, and Gatot Priyanto. "MODEL KINETIKA DEGRADASI CAPSAICIN CABAI MERAH GILING PADA BERBAGAI KONDISI SUHU PENYIMPANAN (Kinetic Model of Capsaicin Degradation on Red Chilli Paste at Various Storage Temperature)." Jurnal Agritech 34, no. 03 (October 24, 2014): 330. http://dx.doi.org/10.22146/agritech.9462.
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The objective of this research was to asses relationship between temperature and storage time of capsaicin degradation of red chilli paste and to measure activation energy and shelf life using the Arrhenius model. The treatmens were storage temperature (20°C, 30°C, 40°C) and storage times (0, 2, 4, 6, 8, 10 weeks). Parameters analyzed were capsaicin content using HPLC method, pH, and particle size. The data was analyzed using linier regression and Arrhenius equation The results showed that temperature condition and storage time affected capsaicin degradation of red chilli paste, unlike pH and particle size. The longer storage time the lower capsaicin content. The capsaicin content of red chilli paste storedat 30°C and 40°C in week-4 was 746,36 μg/g and 714,19 μg/g respectively, and it declined to 149,31 μg/g and 136,77 μg/g after being stored for ten weeks. Research concluded that red chilli paste stored for 10 weeks at 20°C caused the lowest capsaicin degradation from 916.8029 μg/g to 683.8097 μg/g. Degradation rate of capsaicin followed the first order reaction. Arrhenius equation for capsaicin was Y= -9356.3x + 27.836, (R=0.76), and activation energy was 18.581 kcal/mol. Shelf life determination of capsaicin followed kinetic reaction equation of the fi rst order i.e t = ln(Ao-At)/k. The self life of red chilli paste stored at 20°C, 30°C and 40°C were 10.62 weeks, 8.62 weeks and 8.45 weeks respectively.Keywords: Red chilli paste, degradation, capsaicin, particle size, kinetic reaction ABSTRAKTujuan penelitian untuk mengkaji hubungan suhu dan lama penyimpanan terhadap degradasi capsaicin cabai merah giling serta menghitung energi aktivasi dan waktu simpan dengan pendekatan model persamaan Arrhenius. Perlakuan terdiri dari dua faktor yaitu suhu penyimpanan (20°C, 30°C, dan 40°C) serta lama penyimpanan (0, 2, 4, 6, 8 dan 10minggu). Metode analisis untuk kadar capsaicin menggunakan HPLC. Analisis pendukung yaitu pH dan ukuran partikel. Data disajikan dengan grafi k persamaan regresi linier dan persamaan Arrhenius. Hasil penelitian menunjukkan bahwa kondisi suhu dan lama penyimpanan berpengaruh terhadap degradasi capsaicin cabai merah giling, namun, pH dan ukuran partikel tidak berpengaruh secara signifi kan. Semakin lama penyimpanan maka kandungan capsaicin semakin menurun. Kadar capsaicin cabai giling yang disimpan pada suhu 30°C dan 40°C pada minggu ke-empat masing masing sebesar 746,36 μg/g dan 714,19 μg/g menurun perlahan sampai pada minggu ke-10 menjadi 149,31 μg/g dan 136,77 μg/g. Dari hasil penelitian disimpulkan bahwa kadar capsaicin cabai giling yang disimpan pada suhu 20°C selama 10 minggu merupakan degradasi terendah dari 916,80 μg/g menjadi 683,81 μg/g. Laju degradasi capsaicin mengikuti orde satu. Persamaan Arrhenius untuk Capsaicin adalah Y= 27,836-9356,3x (R=0,76) dan energi aktivasisebesar 18581,65 kal/mol. Penentuan umur simpan capsaicin mengikuti persamaan kinetika reaksi orde satu yaitu t =ln(Ao-At)/k, maka umur simpan capsaicin cabai merah giling yang disimpan pada suhu 20°C, 30°C dan 40°C berturutturut sebesar 10,64 minggu; 8,62 minggu dan 8,45 minggu.Kata kunci: Cabai merah giling, degradasi, capsaicin, ukuran partikel, kinetika reaksi
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Lippe, I. T., W. Sametz, K. Sabin, and P. Holzer. "Inhibitory role of capsaicin-sensitive afferent neurons and nitric oxide in hemostasis." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 6 (December 1, 1993): H1864—H1868. http://dx.doi.org/10.1152/ajpheart.1993.265.6.h1864.
Full textAbstract:
Capsaicin-sensitive afferent neurons control blood flow via release of peptide transmitters and formation of nitric oxide (NO). The present study examined whether capsaicin-sensitive afferent neurons and NO interact in the control of hemostasis. Afferent nerve ablation by pretreating rats with a neurotoxic dose of capsaicin (125 mg/kg) led to a 26% reduction of the time of bleeding from punctured small mesenteric arteries in pentobarbital-anesthetized animals. Blockade of NO formation by NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg) attenuated the bleeding time in capsaicin-pretreated rats but had no effect in vehicle-pretreated rats. Platelet aggregation induced by ADP was significantly augmented by 12% in capsaicin-pretreated rats. L-NAME did not alter platelet aggregation in vehicle-pretreated rats but enhanced it in capsaicin-pretreated animals. The prothrombin and partial thromboplastin time and the plasma levels of fibrinogen and antithrombin III remained unchanged by capsaicin or L-NAME, whereas the thrombin time was reduced in capsaicin-pretreated rats. These data indicate that capsaicin-sensitive afferent neurons play an inhibitory role in platelet aggregation and hemostasis, a function in which they interact with the NO system.