Journal articles on the topic 'In vivo experiments on rats'
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Švorc, P., and P. Švorc. "General Anesthesia and Electrocardiographic Parameters in in vivo Experiments Involving Rats." Physiological Research, no. 2 (April 30, 2022): 177–92. http://dx.doi.org/10.33549/physiolres.934848.
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In in vivo cardiovascular or toxicological studies involving rat models, changes in selected electrocardiographic (ECG) parameters are monitored after various interventions to assess the origin and development of heart rhythm disorders. Each ECG parameter has diagnostic significance; as such, commonly evaluated ECG parameters, including heart rate, PR interval, P wave duration, P wave amplitude, QRS complex, QT and QTc interval duration, R wave and T wave amplitude, of rats under various types of general anesthesia were the focus of this study. Studies that performed in vivo cardiovascular or toxicological experiments in rats were retrieved from a search of the Web of Science database for articles published mainly between 2000 and 2021. In total, the search retrieved 123 articles. ECG parameters that were reported as baseline or control values were summarized and averages with ranges were calculated. It is important to be cautious when interpreting results and, in discussions addressing the mechanisms underlying a given type of arrhythmia, acknowledge that initial ECG parameters may already be affected to some extent by the general anesthesia as well as by sex and the time of day the experiments were performed.
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Jourdan, M., L. Cynober, C. Moinard, M. C. Blanc, N. Neveux, J. P. De Bandt, and C. Aussel. "Splanchnic sequestration of amino acids in aged rats: in vivo and ex vivo experiments using a model of isolated perfused liver." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 3 (March 2008): R748—R755. http://dx.doi.org/10.1152/ajpregu.00291.2007.
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Splanchnic sequestration of amino acids (SSAA) is a process observed during aging that leads to decreased peripheral amino acid (AA) availability. The mechanisms underlying SSAA remain unknown. The aim of the present study was to determine whether a high-protein diet could increase nitrogen retention in aged rats by saturating SSAA and whether SSAA could be explained by dysregulation of hepatic nitrogen metabolism. Adult and aged male Sprague-Dawley rats were housed in individual metabolic cages and fed a normal-protein (17% protein) or high-protein diet (27%) for 2 wk. Nitrogen balance (NB) was calculated daily. On day 14, livers were isolated and perfused for 90 min to study AA and urea fluxes. NB was lower in aged rats fed a normal-protein diet than in adults, but a high-protein diet restored NB to adult levels. Isolated perfused livers from aged rats showed decreased urea production and arginine uptake, together with a release of alanine (vs. uptake in adult rats) and a hepatic accumulation of alanine. The in vivo data suggest that SSAA is a saturable process that responds to an increase in dietary protein content. The hepatic metabolism of AA in aged rats is greatly modified, and urea production decreases. This result refutes the hypothesis that SSAA is associated with an increase in AA disposal via urea production.
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Dmytrukha, N. M., S. P. Lugovskoy, and O. S. Lahutina. "Assessment of Fe2O3 nanoparticles impact on functional activity of rats’ peritoneal macrophages in experiments in vitro and in vivo." Ukrainian Journal of Occupational Health 2015, no. 3 (September 30, 2015): 28–33. http://dx.doi.org/10.33573/ujoh2015.03.028.
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Zupkó, I., R. Gaspár, L. Kovács, and G. Falkay. "Are α-adrenergic antagonists potent tocolytics? In vivo experiments on postpartum rats." Life Sciences 61, no. 11 (August 1997): PL159—PL163. http://dx.doi.org/10.1016/s0024-3205(97)00619-x.
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Alimohammadi, Hessamedin, and Wayne L. Silver. "Nasal Chemesthesis: Similarities Between Humans and Rats Observed in In Vivo Experiments." Chemosensory Perception 8, no. 2 (August 2015): 85–95. http://dx.doi.org/10.1007/s12078-015-9189-4.
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Trujillo-Pisanty, Ivan, Christian Sanio, Nadia Chaudhri, and Peter Shizgal. "Robust optical fiber patch-cords for in vivo optogenetic experiments in rats." MethodsX 2 (2015): 263–71. http://dx.doi.org/10.1016/j.mex.2015.05.003.
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Braga, Angélica de Fátima de Assunção, Caroline Coutinho de Barcelos, Franklin Sarmento da Silva Braga, Samanta Cristina Antoniassi Fernandes, Yoko Oshima Franco, Mario Mantovani, and Léa Rodrigues Simioni. "Phenobarbital influence on neuromuscular block produced by rocuronium in rats." Acta Cirurgica Brasileira 23, no. 4 (August 2008): 343–47. http://dx.doi.org/10.1590/s0102-86502008000400008.
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PURPOSE: To evaluate in vitro and in vivo neuromuscular blockade produced by rocuronium in rats treated with Phenobarbital and to determine cytochrome P450 and cytochrome b5 concentrations in hepatic microsomes. METHODS: Thirty rats were included in the study and distributed into 6 groups of 5 animals each. Rats were treated for seven days with phenobarbital (20 mg/kg) and the following parameters were evaluated: 1) the amplitude of muscle response in the preparation of rats exposed to phenobarbital; 2) rocuronium effect on rat preparation exposed or not to phenobarbital; 3) concentrations of cytochrome P450 and cytochrome b5 in hepatic microsomes isolated from rats exposed or not to phenobarbital. The concentration and dose of rocuronium used in vitro and in vivo experiments were 4 µg/mL and 0,6 mg/kg, respectively. RESULTS: Phenobarbital in vitro and in vivo did not alter the amplitude of muscle response. The neuromuscular blockade in vitro produced by rocuronium was significantly different (p=0.019) between exposed (20%) and not exposed (60%) rats; the blockade in vivo was significantly greater (p=0.0081) in treated rats (93.4%). The enzymatic concentrations were significantly greater in rats exposed to phenobarbital. CONCLUSIONS: Phenobarbital alone did not compromise neuromuscular transmission. It produced enzymatic induction, and neuromuscular blockade in vivo produced by rocuronium was potentiated by phenobarbital.
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Yakimova, Krassimira S., Rumen P. Nikolov, Ivan G. Todorov, and Milen H. Hristov. "Leptin and Gaba Interactions on Thermoregulation of Rats." Journal of Biomedical and Clinical Research 7, no. 1 (November 1, 2014): 20–24. http://dx.doi.org/10.1515/jbcr-2015-0120.
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Abstract Leptin inhibits feeding, reduces body weight and increases thermogenesis. Experimental data suggest involvement of GABAergic mechanisms in the regulation of feeding behavior and energy balance. The present study was set to determine the effect of combinations from leptin, GABAB-agonist baclofen and GABAB-antagonist CGP35348 on thermoregulation of male Wistar rats, using in vivo and in vitro experiments. The substances used for in vivo experiments were administered intraperitoneally (i.p.). The measurement of the body temperature was done via thermistor probes (TX8) and monitored on multichannel recorder Iso-Thermex16. In vitro experiments were conducted on rat PO/AH neurons, recorded extracellulary by conventional electrophysiological equipment, using brain slice preparations. The separate intraperitoneal injection of leptin as well as GABAB-antagonist CGP35348 produced significant hyperthermia in rats while the GABAB-agonist baclofen caused a decrease in the core body temperature. The probable synergy between the hyperthermic effects of leptin and GABAB-antagonist did not occur. On the contrary, the effect of this combination was lower as compared to the result of the separate administration of GABAB-antagonist. When leptin was applied just prior to GABAB-agonist baclofen, neither of their separate effects appeared. In vivo effects determined correlated with in vitro changes of firing rate observed in PO/AH neurons. The data from this study provide a new point of view concerning the interactions of leptin and GABA on the level of thermoregulation. These results represent a step forward in understanding the complicated mechanisms involved in thermoregulation.
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Colugnati, Diego B., Ricardo M. Arida, Roberta M. Cysneiros, Vera C. Terra, Eliza Y. F. Sonoda, Aline P. Pansani, Carla A. Scorza, Esper A. Cavalheiro, and Fulvio A. Scorza. "Carbamazepine does not alter the intrinsic cardiac function in rats with epilepsy." Arquivos de Neuro-Psiquiatria 68, no. 4 (August 2010): 573–78. http://dx.doi.org/10.1590/s0004-282x2010000400018.
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Among the causes for sudden unexpected death (SUDEP) in epilepsy, the effects of antiepileptic drugs on the heart have been poorly explored. Based on this, the aim of our study was to evaluate the heart rate (in vivo and isolated ex vivo) and ventricular pressure (isolated ex vivo) of rats with and without epilepsy treated with carbamazepine. Four groups of adult, male Wistar rats (200-250 g) were studied: [A] control rats (n=8), received neither pilocarpine nor carbamazepine [B] carbamazepine-treated rats (n=8), received a daily dose of 120 mg/Kg, i.p. of carbamazepine for two weeks; [C] rats with epilepsy that received just saline solution (n=8); [D] rats with epilepsy that received a daily dose of 120 mg/Kg, i.p. of carbamazepine for two weeks (n=8). Our results showed significant increase in heart rate in animals with epilepsy (with and without the use of carbamazepine) when compared to the control groups in vivo. In contrast, we did not find differences during isolated ex vivo experiments comparing animals with and without epilepsy and despite the use of carbamazepine. Our results suggest that, in isolation, carbamazepine may not be a potential risk factor for sudden unexpected death in epilepsy.
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Verbanck, S., N. Gonzalez Mangado, G. Peces-Barba, and M. Paiva. "Multiple-breath washout experiments in rat lungs." Journal of Applied Physiology 71, no. 3 (September 1, 1991): 847–54. http://dx.doi.org/10.1152/jappl.1991.71.3.847.
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Multiple-breath washouts were performed on 30 Wistar rats postmortem in a study in which breaths of 90% O2–5% He-5% SF6 were given. Preliminary comparison of alveolar plateau slopes obtained from anesthetized rats in vivo and postmortem showed that ventilation distribution remains the same within 1 h after the animals were killed. For maneuvers with different preinspiratory lung volumes and end-inspiratory breathholding, we computed the normalized N2 slope (Sn) and Fowler and Bohr dead spaces [VDF(n) and VDB(n), respectively] as a function of breath number (n). For all maneuvers analyzed, Sn of all gases increased in the first two or three breaths and reached a horizontal asymptote thereafter. The value of Sn decreased, both with increasing preinspiratory lung volume and breath hold of 4 s. The fact that the horizontal Sn asymptote is reached after only two or three breaths suggests the absence of convection-dependent inhomogeneities (CDI) in rat lungs. This contrasts with multiple-breath washout experiments in humans, where interregional (gravity-dependent CDI) and intraregional CDI generate a marked increase in Sn throughout the entire washout. Also, in contrast with results in humans, VDF and VDB were independent of n. The present work suggests that rats may be used to study diffusion- and convection-dependent inhomogeneities without the influence of CDI or gas exchange.
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Ferreira, Luis D. M. C. B., T. Norman Palmer, and Paul A. Fournier. "Prolonged exposure to halothane and associated changes in carbohydrate metabolism in rat muscles in vivo." Journal of Applied Physiology 84, no. 4 (April 1, 1998): 1470–74. http://dx.doi.org/10.1152/jappl.1998.84.4.1470.
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Halothane, an anesthetic presently used in animal experimentation, is reported to stimulate glycogen breakdown in isolated preparations of rat skeletal muscles, suggesting that it may not be a suitable anesthetic for the study of glycogen metabolism in rats in vivo. The purpose of this study was to establish whether prolonged exposure to halothane in rats in vivo is associated with accelerated glycogenolysis. Exposure of rats to halothane for up to 1 h was not accompanied by either any change in the levels of glycogen or increase in activity ratios of glycogen phosphorylase in muscles, irrespective of their fiber compositions. In marked contrast, the levels of lactate, inorganic phosphate, glucose 1-phosphate, glucose 6-phosphate, fructose 1,6-bisphosphate, and fructose 2,6-bisphosphate changed progressively during anesthesia. Accordingly, the interpretation of muscle metabolite levels must be performed with caution in experiments involving prolonged exposure to halothane. Overall, our findings indicate that the reported halothane-mediated stimulation of glycogen breakdown in vitro is likely to be an artifact and that halothane is a suitable anesthetic for experiments concerned with glycogen metabolism in rats.
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Tomenendalova, J., J. Mayer, M. Doubek, D. Horky, K. Rehakova, and J. Doubek. "Chlorambucil and fludarabine as a new pre-transplant conditioning for patients with chronic lymphocytic leukemia: results of in vivo experiments." Veterinární Medicína 53, No. 10 (November 4, 2008): 564–71. http://dx.doi.org/10.17221/1967-vetmed.
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Chronic lymphatic leukemia (CLL), incurable by standard treatments, may be potentially cured by allogeneic hematopoietic stem cell transplantation. Since CLL affects predominantly older people, there is a need for some low-toxicity conditioning with, on the other hand, strong antileukemic activity. Since there are very encouraging results with busulfan + fludarabine conditionings in myeloid malignancies and since the clinical study with the combination treatment with chlorambucil and fludarabine was stopped prematurely for myelotoxicity, we hypothesized that this chlorambucil + fludarabine combination would have the potential as a good conditioning for high-risk lymphoid malignancies. The aim of this study was to test the chlorambucil + fludarabine combination <I>in vivo</I> (in rats) for toxicity. Male Wistar rats were used in all experiments. First, the maximum tolerated dose (MTD) of each drug was tested. For fludarabine, doses of 0.75–60 mg/kg/day, and for chlorambucil, doses of 0.15–50 mg/kg/day were used, all administered for five days. Then, the combination treatment was tested: (1) fludarabine and chlorambucil simultaneously (F+CH), (2) fludarabine followed by chlorambucil (F-CH), (3) chlorambucil followed by fludarabine (CH-F); all drugs were administered for five days. For fludarabine alone, the MTD was not reached. Clinically, the rats tolerated well even the highest doses. Moreover, no myelotoxicity was seen. However, pneumotoxicity, hepatotoxicity, nephrotoxicity, and gastrointestinal toxicity were found by a histological examination. For chlorambucil alone, the MTD is about 40–50 mg/kg/day. Pneumotoxicity, nephrotoxicity, gastrointestinal toxicity, and myelotoxicity were observed. The combination treatment tested a fixed dose of fludarabine (3 mg/kg per day) and three doses of chlorambucil (1, 2, and 4 mg/kg/day). Clinically, the best tolerated combination was fludarabine followed by chlorambucil (F-CH). Haematological toxicity was observed, usually affecting predominantly lymphocytes, and interestingly, it was most pronounced in the clinically best tolerated regimen. Rats can tolerate extremely high doses of fludarabine and chlorambucil. Based on these experiments, for further development, hopefully into the clinical usage, we could recommend the administration of fludarabine, followed by chlorambucil. This combination will further be tested together with monoclonal antibodies and total lymphoid irradiation as a conditioning regimen for allogeneic bone marrow transplantation.
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Akl, Tony J., Takashi Nagai, Gerard L. Coté, and Anatoliy A. Gashev. "Mesenteric lymph flow in adult and aged rats." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (November 2011): H1828—H1840. http://dx.doi.org/10.1152/ajpheart.00538.2011.
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The objective of study was to evaluate the aging-associated changes, contractile characteristics of mesenteric lymphatic vessels (MLV), and lymph flow in vivo in male 9- and 24-mo-old Fischer-344 rats. Lymphatic diameter, contraction amplitude, contraction frequency, and fractional pump flow, lymph flow velocity, wall shear stress, and minute active wall shear stress load were determined in MLV in vivo before and after Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME) application at 100 μM. The active pumping of the aged rat MLV in vivo was found to be severely depleted, predominantly through the aging-associated decrease in lymphatic contractile frequency. Such changes correlate with enlargement of aged MLV, which experienced much lower minute active shear stress load than adult vessels. At the same time, pumping in aged MLV in vivo may be rapidly increased back to levels of adult vessels predominantly through the increase in contraction frequency induced by nitric oxide (NO) elimination. Findings support the idea that in aged tissues surrounding the aged MLV, the additional source of some yet unlinked lymphatic contraction-stimulatory metabolites is counterbalanced or blocked by NO release. The comparative analysis of the control data obtained from experiments with both adult and aged MLV in vivo and from isolated vessel-based studies clearly demonstrated that ex vivo isolated lymphatic vessels exhibit identical contractile characteristics to lymphatic vessels in vivo.
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Klyueva, N. N., I. V. Okunevich, N. S. Parfenova, E. V. Belova, and E. V. Ageeva. "Effect of lipid-lowering activity of the natural original enzyme preparation in the experiment." Biomeditsinskaya Khimiya 65, no. 3 (2019): 227–30. http://dx.doi.org/10.18097/pbmc20196503227.
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The experimental study in vivo was aimed at evaluation of hypolipidemic action of the original natural microbial enzyme preparation of cholesterol oxidase (CHO). In preliminary chronic experiments in rats, rabbits, dogs, low toxicity, good tolerability, and anti-atherosclerotic activity of the CHO preparation were established. To assess the effect of CHO under conditions of moderate, nutritional, atherogenic dyslipoproteinemia, experiments were carried out in rats, guinea pigs, and rabbits. It was shown that administration of CHO had the pronounced lipid-lowering effect in models of atherogenic dyslipoproteinemia induced in these animals.
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Ying, Wei-Zhong, Kristal J. Aaron, and Paul W. Sanders. "Sodium and potassium regulate endothelial phospholipase C-γ and Bmx." American Journal of Physiology-Renal Physiology 307, no. 1 (July 1, 2014): F58—F63. http://dx.doi.org/10.1152/ajprenal.00615.2013.
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The amount of Na+ and K+ in the diet promotes significant changes in endothelial cell function. In the present study, a series of in vitro and in vivo experiments determined the role of Na+ and K+ in the regulation of two pleckstrin homology domain-containing intracellular signaling molecules, phospholipase C (PLC)-γ1 and epithelial and endothelial tyrosine kinase/bone marrow tyrosine kinase on chromosome X (Bmx), and agonist-generated Ca2+ signaling in the endothelium. Extracellular K+ concentration regulated the levels of activated PLC-γ1, Bmx, and carbachol-stimulated intracellular Ca2+ mobilization in human endothelial cells. Additional experiments confirmed that high-conductance Ca2+-activated K+ channels and phosphatidylinositol 3-kinase mediated these effects. The content of Na+ and K+ in the diet also regulated Bmx levels in endothelial cells and activated PLC-γ1 levels in rats in vivo. The effects of dietary K+ on Bmx were more pronounced in rats fed a high-salt diet compared with rats fed a low-salt diet. These experiments elucidated an endothelial cell signaling mechanism regulated by electrolytes, further demonstrating an integral relationship between endothelial cell function and dietary Na+ and K+ content.
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Osmond, David A., and Edward W. Inscho. "P2X1 receptor blockade inhibits whole kidney autoregulation of renal blood flow in vivo." American Journal of Physiology-Renal Physiology 298, no. 6 (June 2010): F1360—F1368. http://dx.doi.org/10.1152/ajprenal.00016.2010.
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In vitro experiments demonstrate that P2X1 receptor activation is important for normal afferent arteriolar autoregulatory behavior, but direct in vivo evidence for this relationship occurring in the whole kidney is unavailable. Experiments were performed to test the hypothesis that P2X1 receptors are important for autoregulation of whole kidney blood flow. Renal blood flow (RBF) was measured in anesthetized male Sprague-Dawley rats before and during P2 receptor blockade with PPADS, P2X1 receptor blockade with IP5I, or A1 receptor blockade with DPCPX. Both P2X1 and A1 receptor stimulation with α,β-methylene ATP and CPA, respectively, caused dose-dependent decreases in RBF. Administration of either PPADS or IP5I significantly blocked P2X1 receptor stimulation. Likewise, administration of DPCPX significantly blocked A1 receptor activation to CPA. Autoregulatory behavior was assessed by measuring RBF responses to reductions in renal perfusion pressure. In vehicle-infused rats, as pressure was decreased from 120 to 100 mmHg, there was no decrease in RBF. However, in either PPADS- or IP5I-infused rats, each decrease in pressure resulted in a significant decrease in RBF, demonstrating loss of autoregulatory ability. In DPCPX-infused rats, reductions in pressure did not cause significant reductions in RBF over the pressure range of 100–120 mmHg, but the autoregulatory curve tended to be steeper than vehicle-infused rats over the range of 80–100 mmHg, suggesting that A1 receptors may influence RBF at lower pressures. These findings are consistent with in vitro data from afferent arterioles and support the hypothesis that P2X1 receptor activation is important for whole kidney autoregulation in vivo.
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GUIMARÃES, CARINE A., MAIRIS S. BIELLA, ABIGAIL LOPES, PEDRO F. DEROZA, MARIANA B. OLIVEIRA, TAMIRES P. MACAN, EMILIO L. STRECK, GUSTAVO C. FERREIRA, ALEXANDRA I. ZUGNO, and PATRÍCIA F. SCHUCK. "In vivo and in vitro effects of fructose on rat brain acetylcholinesterase activity: an ontogenetic study." Anais da Academia Brasileira de Ciências 86, no. 4 (December 2014): 1919–26. http://dx.doi.org/10.1590/0001-3765201420140173.
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Increased fructose concentrations are the biochemical hallmark of fructosemia, a group of inherited disorders on the metabolic pathway of this sugar. The main clinical findings observed in patients affected by fructosemia include neurological abnormalities with developmental delay, whose pathophysiology is still undefined. In the present work we investigated the in vitro and in vivo effects of fructose on acetylcholinesterase (AchE) activity in brain structures of developing rats. For the in vitro experiments, fructose was added at increasing concentrations to the incubation medium. It was observed that fructose provoked an inhibition of acetylcholinesterase activity in cerebral cortex of 30-day-old-rats, even at low concentrations (0.1 mM). For the in vivo experiments, rats were killed 1 h after a single fructose administration (5 µmol/g). Control group received the same volume of saline solution. We found that AchE activity was increased in cerebral cortex of 30- and 60-day-old rats receiving fructose administration. Finally, we observed that AchE activity was unaffected by acute fructose administration in cerebral cortex, striatum or hippocampus of 15- and 90-day-old rats. The present data suggest that a disruption in cholinergic homeostasis may be involved in the pathophysiology of brain damage observed in young patients affected by fructosemia.
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Walker, B. R., J. Haynes, H. L. Wang, and N. F. Voelkel. "Vasopressin-induced pulmonary vasodilation in rats." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 2 (August 1, 1989): H415—H422. http://dx.doi.org/10.1152/ajpheart.1989.257.2.h415.
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Experiments were performed to determine the pulmonary vascular responses to exogenous or endogenous arginine vasopressin (AVP) in rats. Both in vitro and in vivo approaches were used to examine the direct pulmonary vasoactive properties of AVP and how those properties affect pulmonary hemodynamics in the intact animal. In conscious, unrestrained rats, constant infusion of AVP (4.0 mU.kg-1.min-1 iv) resulted in a fall in mean pulmonary artery pressure (PAP), although systemic pressure was increased. Coincident with the fall in PAP were similar reductions in cardiac output and heart rate. Similarly, bolus administration of AVP reduced PAP, and this effect was augmented during hypoxia. Another series of experiments examined the effect of endogenous AVP released by arterial hypoxemia on pulmonary hemodynamics in conscious rats. Administration of a specific V1-vasopressinergic antagonist had no effect on the PAP response to hypoxia; however, systemic resistance tended to fall following V1-antagonism. To determine the vasoactive properties of AVP independent of these changes in blood flow, a series of experiments were performed on isolated, perfused rat lungs. Injection of 25, 200, or 2,000 mU of AVP into the circulation of the isolated lung was without effect under normoxic conditions. In contrast, 25 mU AVP elicited reproducible pulmonary vasodilation when injected during ongoing hypoxic pulmonary vasoconstriction. This vasodilatory response was unaffected by meclofenamate or by the platelet-activating factor receptor antagonist SRI 63-441, but was blocked by a specific V1-vasopressinergic antagonist. We conclude that although AVP exerts profound systemic vasoconstriction, the pulmonary circulation appears relatively unaffected by exogenous or endogenous AVP in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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Mac Laughlin, Myriam, María Cristina Damasco, Pilar Igarreta, and Carlos Amorena. "In vitro and in vivo evaluation of proximal tubular acidification in aging rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 6 (June 1, 2001): R1627—R1631. http://dx.doi.org/10.1152/ajpregu.2001.280.6.r1627.
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The normal aging process is accompanied by a progressive deterioration of renal function. We studied the kinetics of proximal tubular acidification of young (3 mo) and aging (22 mo) rats using in vivo and in vitro techniques. Blood acid-base parameters were similar in both groups. The maximum velocity of the Na+/H+ exchange (NHE) in brush-border membrane vesicles (BBMV) showed a 72% decrease in aging compared with young rats, whereas the Michaelis constant remained unchanged. The NHE3 isoform of the Na+/H+ exchanger was detected in BBMV by Western blot in both groups, and a decrease of 90% in the abundance was observed in aging rats. Micropuncture experiments with simultaneous luminal and peritubular perfusion with phosphate Ringer and continuous measurement of intratubular pH showed an acidification rate constant 34% smaller in aging compared with young rats. Proton flux was 48% lower in aging than in young rats. The present results suggest that proximal tubular acidification is impaired with aging.
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D’Angelo, Gerard, Jennifer S. Pollock, and David M. Pollock. "In vivo evidence for endothelin-1-mediated attenuation of α1-adrenergic stimulation." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 3 (March 2006): H1251—H1258. http://dx.doi.org/10.1152/ajpheart.00203.2005.
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Experiments were designed to determine the influence of endothelin A (ETA) receptors on the pressor response to acute environmental stress in Dahl salt-resistant (DR) and Dahl-sensitive (DS) rats. Mean arterial pressure (MAP) was chronically monitored by telemetry before and after treatment with the selective ETA receptor antagonist ABT-627. Rats were restrained and subjected to pulsatile air jet stress (3 min). In untreated animals, the total pressor response (area under the curve) to acute stress was not different between DR vs. DS rats (8.1 ± 1.7 vs. 15.6 ± 2.6 mmHg × 3 min, P = 0.10). Conversely, treatment with ABT-627 potentiated the total pressor response only in DR rats (36.3 ± 6.2 vs. 22.6 ± 5.9 mmHg × 3 min, DR vs. DS, P < 0.05). Treatment with ABT-627 allowed greater responses in anesthetized DR rats to exogenous phenylephrine (1–4 μg/kg) during ganglionic blockade ( P < 0.05) and produced a significant increase in plasma norepinephrine at baseline and during stress in conscious DR rats compared with untreated animals ( P < 0.05). ETA receptor blockade had no effect on these responses in DS rats. Our results suggest that endothelin-1 can inhibit α-adrenergic-mediated effects in DR, but not DS rats, consistent with the hypothesis that ETA receptor activation functions to reduce sympathetic nerve activity and responses in vascular smooth muscle to sympathetic stimulation.
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Islam, Jahid M. M., Md Ismail, Md Rakibul Islam, Md Faruk Hossain, and Hossain Uddin Shekhar. "Boosting the Food Functionality (In Vivo and In Vitro) of Spirulina by Gamma Radiation: An Inspiring Approach." International Journal of Food Engineering 11, no. 4 (August 1, 2015): 579–85. http://dx.doi.org/10.1515/ijfe-2014-0342.
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Abstract Foods (natural or processed) containing known biologically active compounds, which supplies clinically established and well-documented health benefits, are termed as functional food. Study objectives were to boost food functionality of spirulina, to optimize the required radiation dose, and to test functionality of spirulina both in vitro and in vivo. For this purpose fat binding capacity, sugar binding capacity, hydration property, antioxidative property, total polyphenol content were assessed at different radiation doses. A total of 30 rats were divided into three groups to carry out in vivo experiments to validate the outcomes of in vitro experiments. Targeted physico-chemical properties of spirulina were increased at their maximum level at 15 kGy radiation dose. In vivo experiments validated the outcomes of in vitro experiments. Though gamma radiation improves food functionality of spirulina at various radiation doses, but the optimum dose is recommended as 15 kGy.
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Zhukova, Galina Vitalyevna, Alla Ivanovna Shikhlyarova, Tatiana Albertovna Barteneva, Marina Igorevna Bragina, Elena Alekseevna Shirnina, Oleg Evgenevich Polozhentsev, and Tatiana Anatolevna Kurkina. "Factors and conditions affecting the antitumor effect of magnetite nanoparticles in the experiments in vivo." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e14051-e14051. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e14051.
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e14051 Background: Independent antitumor effects of magnetite nanoparticles (NPs) in animals, up to complete regression of large tumors, have been demonstrated. Factors and conditions that contribute to the appearance and enhancement of such effects are an important issue. Our purpose was to study the dependence of antitumor effects of magnetite NPs on characteristics of animals, ways of preparation and injection of NPs and weak magnetic fields (WMF). Methods: The experiment included 380 white outbred rats with transplantable sarcoma 45 (S45), Pliss lymphosarcoma (PL) and Heren carcinoma (HC) and 230 С57Black/6 mice with B16 melanoma. The animals received 6-8 1.25-35.4 mg/kg peritumoral or intraperitoneal injections of a water-based magnetite NP ferrofluid (FF) diluted with saline solution. WMF parameters were: 0.03-9 Hz frequency, 0.7-3.2 mT induction, exposure on the head. Dynamics of tumor sizes, histological changes and FF characteristics after the dilution with saline (X-ray absorption spectroscopy analysis) were evaluated. Results: An effective single dose in S45 female rats with peritumoral injections was higher than in males (35.4 and 17.7 mg/kg, respectively). Female rats with HC were sensitive to small NP doses (1.25 mg/kg) in intraperitoneal (but not peritumoral) injections (regression in > 30%). Peritumoral injections of small NP doses were most effective in PL males, while a number of experiments did not show benefits of small NP doses for mice. NP solution storage led to its lower effect due to the oxidation of Fe +2 to Fe +3, and even FF dilution ex tempora decreased the effect as SS pH changed to 7.4. WMF was able to enhance the effect of NPs by up to 1.5 times but not in intraperitoneal injections. Conclusions: Antitumoral effects of NPs depended on species of animals and their gender, tumor types, doses and methods of NP injections, storage time of diluted FF prior to its injection, saline pH, and WMF. WMF effects were different depending on NP injection methods.
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Park, HyungDal, Wonsuk Choi, Seonghwan Oh, Yong-Jun Kim, Seonho Seok, and Jinseok Kim. "A Study on Biocompatible Polymer-Based Packaging of Neural Interface for Chronic Implantation." Micromachines 13, no. 4 (March 26, 2022): 516. http://dx.doi.org/10.3390/mi13040516.
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This paper proposed and verified the use of polymer-based packaging to implement the chronic implantation of neural interfaces using a combination of a commercial thermal epoxy and a thin parylene film. The packaging’s characteristics and the performance of the vulnerable interface between the thermal epoxy layer and polyimide layer, which is mainly used for neural electrodes and an FPCB, were evaluated through in vitro, in vivo, and acceleration experiments. The performance of neural interfaces—composed of the combination of the thermal epoxy and thin parylene film deposition as encapsulation packaging—was evaluated by using signal acquisition experiments based on artificial stimulation signal transmissions through in vitro and in vivo experiments. It has been found that, when commercial thermal epoxy normally cured at room temperature was cured at higher temperatures of 45 °C and 65 °C, not only is its lifetime increased with about twice the room-temperature-based curing conditions but also an interfacial adhesion is higher with more than twice the room-temperature-based curing conditions. In addition, through in vivo experiments using rats, it was confirmed that bodily fluids did not flow into the interface between the thermal epoxy and FPCB for up to 18 months, and it was verified that the rats maintained healthy conditions without occurring an immune response in the body to the thin parylene film deposition on the packaging’s surface.
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Okunevich, Irina V., Natalia N. Klyueva, Nina S. Parfenova, and Elena V. Belova. "Lipid-lowering and anti-atherosclerotic activity of the natural original enzyme preparation in the experiment." Reviews on Clinical Pharmacology and Drug Therapy 17, no. 3 (September 21, 2019): 79–84. http://dx.doi.org/10.17816/rcf17379-84.
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The experimental large-scale investigation in vitro and in vivo is devoted to the results of a long-term study of the biological, lipid-lowering and anti-atherosclerotic activity of the original natural microbial enzyme preparation of cholesterol oxidase (CHO). In chronic experiments (rats, rabbits, dogs), low toxicity, good tolerability, and anti-atherosclerotic activity of the CHO preparation were established. To assess the effect of CHO in conditions of moderate nutritional dyslipoproteinemia, experiments were carried out in 3 species of animals (rats, guinea pigs, rabbits). It was shown the pronounced lipid-lowering effect of CHO in modeling dyslipoproteinemia.
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Kaviani, Farnoosh, Missagh Jalali, Elham Hoveizi, Javad Jamshidian, and Masumeh Ahmadizadeh. "Montelukast Protects Against Renal Damage Due to Cadmium Toxicity: In vivo and In vitro Experiments." Iranian Journal of Toxicology 15, no. 4 (October 1, 2021): 223–32. http://dx.doi.org/10.32598/ijt.15.4.422.2.
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Background: The protective effects of Montelukast (Mont), as an anti-inflammatory drug, against cadmium-induced kidney cell damage have already been studied and identified. Since the significant part of cadmium nephrotoxicity is caused by oxidative stress, this in vivo and in vitro study was conducted to investigate the possible role of Montelukast antioxidant properties in the protection. Methods: In the in vivo section, 42 rats were treated in seven groups of six rats as follows: Control; Cadmium Chloride (CdCl2) control; Montelukast control; CdCl2 plus Montelukast treatment; CdCl2 with Montelukast pre-treatment; Vitamin E control; CdCl2 plus Vitamin E treatment. In the in vitro section, human embryonic kidney cells (HEK293) were treated with CdCl2; Montelukast; Combined CdCl2 and Montelukast; Vitamin E; Combined CdCl2 and Vitamin E. Results: Montelukast, in both treatment and pretreatment forms, reduced serum urea, creatinine, and potassium levels compared to CdCl2 group, in vivo. Similar to vitamin E, the pre-treatment with Montelukast was associated with a significant decrease in Nitric Oxide (NO) and Total Antioxidant Capacity (TAC) in serum and renal tissue, and a significant increase in Glutathione Peroxidase (GPX) activity in serum compared those in the CdCl2 group. In the in vitro section of the study, Montelukast significantly reduced Malondialdehyde (MDA) and NO while the TAC level, Superoxide Dismutase (SOD), and the GPX activity increased significantly. Conclusion: Overall, the antioxidant effects of Montelukast appear to play a prominent role in preventing the renal toxicity due to cadmium exposure.
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Melnik, E. A., Yu P. Buzulukov, V. F. Demin, V. A. Demin, I. V. Gmoshinski, N. V. Tyshko, and V. A. Tutelyan. "Transfer of Silver Nanoparticles through the Placenta and Breast Milk during in vivo Experiments on Rats." Acta Naturae 5, no. 3 (September 15, 2013): 107–15. http://dx.doi.org/10.32607/20758251-2013-5-3-107-115.
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Silver nanoparticles (NPs), widely used in the manufacture of various types of consumer products and for medical applications, belong to novel types of materials that pose potential risks to human health. The potential negative effects of the influence of these NPs on reproduction are insufficiently researched. A quantitative assessment of the transfer of metallic silver nanoparticles through the placenta and breast milk was carried out during an in vivo experiment. We used 34.9 14.8 nm in size silver NPs that were stabilized by low-molecularweight polyvinylpyrrolidone and labeled with the 110mAg radioactive isotope using thermal neutron irradiation in a nuclear reactor. [110mAg]-labeled NPs preparations were administered intragastrically via a gavage needle to pregnant (20th day of gestation) or lactating (14-16th day of lactation) female rats at a dose of 1.69-2.21 mg/kg of body weight upon conversion into silver. The accumulation of NPs in rat fetuses and infant rats consuming their mothers breast milk was evaluated using a low-background semiconductor gamma-ray spectrometer 24 and 48 hours following labeling, respectively. In all cases, we observed a penetration of the [110mAg]-labeled NPs through the placenta and ther entry into the mothers milk in amounts exceeding by 100-1,000 times the sensitivity of the utilized analytical method. The average level of accumulation of NPs in fetuses was 0.085-0.147% of the administered dose, which was comparable to the accumulation of the label in the liver, blood, and muscle carcass of adult animals and exceeded the penetration of NPs across the hematoencephalic barrier into the brain of females by a factor of 10-100. In lactating females, the total accumulation of [110mAg]-labeled NPs into the milk exceeded 1.94 0.29% of the administered dose over a 48 h period of lactation; not less than 25% of this amount was absorbed into the gastrointestinal tract of infant rats. Thus, this was the first time experimental evidence of the transfer of NPs from mother to offspring through the placenta and breast milk was obtained.
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Pison, C. M., C. Chauvin, E. Fontaine, F. Catelloni, C. Keriel, B. Paramelle, and X. M. Leverve. "Mechanism of gluconeogenesis inhibition in rat hepatocytes isolated after in vivo hypoxia." American Journal of Physiology-Endocrinology and Metabolism 268, no. 5 (May 1, 1995): E965—E973. http://dx.doi.org/10.1152/ajpendo.1995.268.5.e965.
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Gluconeogenesis was studied in hepatocytes isolated from fasted rats submitted to 24 h of hypoxic exposure (inspired O2 fraction 0.1) or to room air. Hepatocytes from hypoxic rats compared with controls exhibited a lower gluconeogenic rate with lactate (5.1 +/- 0.3 vs. 7.2 +/- 0.3 mumol.min-1.g dry cells-1, P < 0.001) but not with dihydroxyacetone (9.1 +/- 0.3 vs. 9.4 +/- 0.4 mumol.min-1.g dry cells-1), suggesting involvement of the phosphoenolpyruvate-pyruvate cycle. Experiments with perifused hepatocytes from hypoxic and control rats showed a single relationship between phosphoenolpyruvate and glucose flux (JGlc) but two different curves when cytosolic oxalacetate was plotted against JGlc. The decreased phosphoenolpyruvate carboxykinase (PEPCK) activity in the hypoxic group (9.0 +/- 0.9 vs. 16.2 +/- 1.9 nmol.min-1.mg protein-1, P < 001) without change in the Michaelis constant further settled the involvement of this step. The significant decrease in PEPCK mRNA levels in livers from hypoxic rats led us to propose that in vivo hypoxic exposure inhibits gluconeogenesis at the PEPCK level by decreasing PEPCK gene transcription.
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Seiffert, D., M. Geisterfer, J. Gauldie, E. Young, and T. J. Podor. "IL-6 stimulates vitronectin gene expression in vivo." Journal of Immunology 155, no. 6 (September 15, 1995): 3180–85. http://dx.doi.org/10.4049/jimmunol.155.6.3180.
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Abstract We tested the hypothesis that vitronectin (Vn) is regulated as an acute phase reactant in response to inflammatory stimuli. In initial experiments, Vn levels were measured during the surgically induced acute phase response in humans. The plasma concentration of Vn increased approximately twofold following elective orthopedic surgery and remained elevated up to 5 days. To examine the mechanism(s) of increased Vn synthesis, hepatic Vn mRNA expression and serum levels were examined in three rat models of acute inflammation: LPS (i.v.), CFA (i.p.), or turpentine (s.c.) injection. The serum concentration of Vn increased approximately twofold 24 h following treatment with turpentine. The expression of Vn mRNA in the liver increased markedly as early as 3 h after treatment in these models and remained elevated up to 18 h. Northern blot analysis of RNA isolated from fractionated liver cells derived from rats treated with LPS indicated that Vn was mainly expressed in hepatocytes, but not in the endothelial or nonparenchymal cell fractions. To analyze the individual effects of raised corticosterone and IL-6 levels on the expression of hepatic Vn mRNA, rats were injected (i.p.) with either dexamethasone or purified recombinant rat IL-6. Vn mRNA expression was elevated within 1 h after IL-6 injection, whereas dexamethasone-injected rats showed unchanged Vn expression. Vn mRNA also was increased in rats chronically injected with IL-6. These results indicate that the Vn gene is up-regulated in acute and chronic inflammation, and this induction is primarily mediated by IL-6.
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Yang, Wenjiu, Jing Han, Shuo Gong, Jun Zhao, Tengbo Yu, and Jinfeng Ma. "Cryptotanshinone Suppressed Postmenopausal Osteoporosis by Preventing RANKL-Mediated Osteoclastogenesis against Kidney Injury." Evidence-Based Complementary and Alternative Medicine 2022 (January 29, 2022): 1–8. http://dx.doi.org/10.1155/2022/2821984.
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Background. Cryptotanshinone (CPT), an active component extracted from the root of Salvia miltiorrhiza Bunge, exhibits extensive favorable bioactive properties including anti-inflammatory, antioxidative, antibacterial, and antitumor effects. This study aims to investigate the effects of CPT on osteogenesis and explore related mechanisms both in vivo and in vitro. Methods. In the in vivo experiment, ovariectomized (OVX) female rats were intragastrically administered with CPT at doses of 10 mg/kg and 20 mg/kg for 13 consecutive weeks. Dual-energy X-ray absorptiometry was employed to detect bone mineral density (BMD). ELISA assay was leveraged to detect the biochemical parameters such as BUN and creatinine in the kidney samples. Bone and kidney sections were dyed by H&E and Masson staining kits. In the in vitro experiment, the RAW 264.7 cells were stimulated through the receptor activation of the nuclear factor kappa B ligand (RANKL) to establish an osteoclast differentiation model, and CPT’s protective effect against bone loss was evaluated. Differentiated osteoclasts were determined by TRAP staining. While, osteoclast-marker proteins such as NFATc1, c-Fos, and cathepsin K were identified by Western blot. Results. The results from in vivo experiments revealed that CPT could elevate bone mass and increase bone formation markers in OVX rats. Intriguingly, CPT administration noticeably ameliorated the kidney injury in OVX rats by suppressing BUN and restoring creatinine levels. Furthermore, the results from in vitro experiments suggested that CPT downregulated the protein expression of osteoclast-associated genes such as cathepsin K, c-Fos, and NFATc1 which hinted the related potential mechanisms. Conclusion. The evidence from in vivo and in vitro experiments suggested that CPT exerted antiosteoclastogenic effects by inhibiting the activation of osteoclast differentiation followed by suppressing the protein expressions of cathepsin K, c-Fos, and NFATc1 in osteoclast precursors, and it exhibited protective effects against kidney damage, which highlighted its advantage in clinical application.
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Demori, I., C. Bottazzi, and E. Fugassa. "Tri-iodothyronine increases insulin-like growth factor binding protein-2 expression in cultured hepatocytes from hypothyroid rats." Journal of Endocrinology 161, no. 3 (June 1, 1999): 465–74. http://dx.doi.org/10.1677/joe.0.1610465.
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Previous evidence suggests the existence of a thyroid hormone-IGF axis in the liver and changes in hepatic insulin-like growth factor binding protein (IGFBP) expression in rats with altered thyroid status have been previously reported. The aim of this study was to check if the higher IGFBP-2 mRNA levels observed in liver of hypothyroid rats could be due to a direct effect of thyroid hormone on the IGFBP-2 gene. In our experiments, cultured hepatocytes isolated from normal and hypothyroid adult rats were used. Northern blot analysis revealed barely detectable IGFBP-2 mRNA in normal rat hepatocytes, but easily detectable signal in hypothyroid rat cells. Therefore, the effect of tri-iodothyronine (T3) was investigated using cultured hepatocytes from hypothyroid rats as an in vitro model. The IGFBP-2 message was increased in a dose-dependent manner in hepatocytes cultured for 12-24 h in the presence of T3. A similar increase occurred in accumulation of IGFBP-2 in the culture medium, as measured by RIA. The effect of T3 on IGFBP-2 transcript levels appeared to consist of enhanced gene transcription and was independent of ongoing protein synthesis, but it was completely abolished by the incubation of hepatocytes with insulin. The latter result confirmed the dominant role of insulin in regulating IGFBP-2 expression by cultured hepatocytes. In vivo experiments confirmed an increase in hepatic IGFBP-2 mRNA and serum IGFBP-2 levels in hypothyroid rats and demonstrated, in addition, a significant increase in these measures in T3-treated rats. Taken together, our in vitro and in vivo results support a role for a thyroid hormone-IGF axis in the liver and suggest that other factors, such as insulin, interact in vivo with thryoid hormone in regulating hepatic IGFBP-2 expression.
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Julou-Schaeffer, G., G. A. Gray, I. Fleming, C. Schott, J. R. Parratt, and J. C. Stoclet. "Loss of vascular responsiveness induced by endotoxin involves L-arginine pathway." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 4 (October 1, 1990): H1038—H1043. http://dx.doi.org/10.1152/ajpheart.1990.259.4.h1038.
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The involvement of L-arginine-dependent nitric oxide (NO) production in the vascular failure observed in endotoxemia was investigated in male Wistar rats treated with Escherichia coli lipopolysaccharide (LPS). Contractile responses to norepinephrine (NE) were measured ex vivo in aortas isolated from rats treated with LPS (20 mg/kg ip, 4 h before experiments) and pressor responses to NE were recorded in vivo in rats infused with LPS (5 mg.kg-1.h-1 iv). LPS pretreatment induced a rightward shift of the concentration-response curve to NE and a reduction of the maximal contraction by approximately 43% and 54% (P less than 0.05) in aortic rings with and without functional endothelium, respectively. This was not modified by the presence of indomethacin (10 microM) during the contractile experiments. In contrast, in the presence of NG-monomethyl-L-arginine (L-NMMA, 300 microM) or methylene blue (10 microM), maximal contractions to NE were restored to control values whether functional endothelium was present or not. The effects of L-NMMA were reversed by L- but not by D-arginine. Additionally, the effects of LPS pretreatment on vascular contractility were potentiated by L-arginine. In vivo, LPS infusion produced a reduction in pressor responsiveness to NE (0.1-10 mg/kg), which was also abolished by L-NMMA (30 mg/kg iv). This effect of L-NMMA was reversed by L- but not by D-arginine (100 mg/kg iv). These results demonstrate that activation of the L-arginine pathway has a major role in the production of vascular hyporeactivity in endotoxemia, ex vivo as well as in vivo. Additionally, they suggest that endothelium-independent vascular production of NO may be involved.
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Wang, Jiahao, Yuying Sun, and Xiangtong Tian. "The Inhibitory Effect of Icariin Nanoparticles on Angiogenesis in Pulmonary Fibrosis." Journal of Nanoscience and Nanotechnology 21, no. 11 (November 1, 2021): 5429–35. http://dx.doi.org/10.1166/jnn.2021.19316.
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This study investigated icariin (ICA) nanoparticles on angiogenesis in rats with pulmonary fibrosis and its mechanism. First, icariin solid nanoliposomes (ICA-SLN) were prepared. The in vitrorelease of icariin nanoparticles was determined using a UV-Vis spectrophotometer, after which the plasma concentration of icariin nanoparticles in rats was determined. The bioavailability of icariin nanoparticles was investigated, and the effect of icariin on angiogenesis of pulmonary fibrosis rats was re-observed. The results showed that the bioavailability of icariin in vivo was enhanced after nanomodification, which indicated that icariin solid nanoliposome was a good choice for oral sustained-release nanocarrier materials. in vivo experiments showed that icariin could significantly inhibit angiogenesis in rats with pulmonary fibrosis, and the inhibitory effect was related to the dose and time of action. Most importantly, this study provides the possibility of icariin as a targeted agent for future-targeted therapy.
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Zawirska-Wojtasiak, Renata, Agnieszka Fedoruk-Wyszomirska, Paulina Piechowska, Sylwia Mildner-Szkudlarz, Joanna Bajerska, Elżbieta Wojtowicz, Krzysztof Przygoński, Dorota Gurda, Wiktoria Kubicka, and Eliza Wyszko. "β-Carbolines in Experiments on Laboratory Animals." International Journal of Molecular Sciences 21, no. 15 (July 24, 2020): 5245. http://dx.doi.org/10.3390/ijms21155245.
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Some studies have ascribed a protective effect against neurodegenerative diseases to the β-carbolines harman (H) and norharman (NH), which occur mostly in coffee and coffee substitutes. We determined the concentrations of β-carbolines and undesirable compounds (such as acrylamide) in roasted coffee substitute ingredients and found that chicory coffee was optimal. Two in vivo experiments were conducted with seventeen-month-old male Sprague Dawley rats fed a diet with the addition of pure carboline standards in the first stage, and chicory in the second. We observed an increase in the level of H and NH in blood plasma, as well as higher activity of animals in the battery behavioral test, particularly in the second stage. The results of in vitro studies—particularly the level of the expression in brain tissue of genes associated with aging processes and neurodegenerative diseases—clearly show the benefits of a diet rich in β-carbolines.
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Szczech, G. M., P. Furman, G. R. Painter, D. W. Barry, K. Borroto-Esoda, T. B. Grizzle, M. R. Blum, et al. "Safety Assessment, In Vitro and In Vivo, and Pharmacokinetics of Emivirine, a Potent and Selective Nonnucleoside Reverse Transcriptase Inhibitor of Human Immunodeficiency Virus Type 1." Antimicrobial Agents and Chemotherapy 44, no. 1 (January 1, 2000): 123–30. http://dx.doi.org/10.1128/aac.44.1.123-130.2000.
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ABSTRACT Emivirine (EMV), formerly known as MKC-442, is 6-benzyl-1-(ethoxymethyl)-5-isopropyl-uracil, a novel nonnucleoside reverse transcriptase inhibitor that displays potent and selective anti-human immunodeficiency virus type 1 (HIV-1) activity in vivo. EMV showed little or no toxicity towards human mitochondria or human bone marrow progenitor cells. Pharmacokinetics were linear for both rats and monkeys, and oral absorption was 68% in rats. Whole-body autoradiography showed widespread distribution in tissue 30 min after rats were given an oral dose of [14C]EMV at 10 mg/kg of body weight. In rats given an oral dose of 250 mg/kg, there were equal levels of EMV in the plasma and the brain. In vitro experiments using liver microsomes demonstrated that the metabolism of EMV by human microsomes is approximately a third of that encountered with rat and monkey microsomes. In 1-month, 3-month, and chronic toxicology experiments (6 months with rats and 1 year with cynomolgus monkeys), toxicity was limited to readily reversible effects on the kidney consisting of vacuolation of kidney tubular epithelial cells and mild increases in blood urea nitrogen. Liver weights increased at the higher doses in rats and monkeys and were attributed to the induction of drug-metabolizing enzymes. EMV tested negative for genotoxic activity, and except for decreased feed consumption at the high dose (160 mg/kg/day), with resultant decreases in maternal and fetal body weights, EMV produced no adverse effects in a complete range of reproductive toxicology experiments performed on rats and rabbits. These results support the clinical development of EMV as a treatment for HIV-1 infection in adult and pediatric patient populations.
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Zammit, V. A. "Use of in vivo and in vitro techniques for the study of the effects of insulin on hepatic triacylglycerol secretion in different insulinaemic states." Biochemical Society Transactions 28, no. 2 (February 1, 2000): 103–9. http://dx.doi.org/10.1042/bst0280103.
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This review illustrates how the use of several in vitro and in vivo techniques was necessary to show that the effect of insulin on hepatic triacylglycerol (TAG) secretion in the rat depends on the prior physiological state of the animal. The effect of insulin was always inhibitory when cultured cells were used, irrespective of the physiological state of the donor rats. By contrast, when perfused livers were used, insulin stimulated TAG secretion by livers isolated from fed, normoinsulinaemic rats, but inhibited it in livers from fasted or streptozotocin diabetic animals. This switch in insulin action was also shown to occur in vivo in experiments that involved the liver-specific targeting of both insulin (delivered within liposomes) and labelled fatty acids (delivered as cholesteryl esters within very-low-density lipoprotein remnants) in awake, unrestrained rats during a euglycaemic clamp. It is concluded that observations obtained with perfused liver preparations are more representative of the actual changes that occur in vivo with respect to the effects of insulin on hepatic TAG secretion.
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Tomosugi, N. I., S. J. Cashman, H. Hay, C. D. Pusey, D. J. Evans, A. Shaw, and A. J. Rees. "Modulation of antibody-mediated glomerular injury in vivo by bacterial lipopolysaccharide, tumor necrosis factor, and IL-1." Journal of Immunology 142, no. 9 (May 1, 1989): 3083–90. http://dx.doi.org/10.4049/jimmunol.142.9.3083.
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Abstract We have investigated the effects of LPS, human rTNF (hrTNF) and human rIL-1 beta (hrIL-1 beta) pretreatment on the intensity of antibody-mediated injury in vivo by using a passive model of anti-glomerular basement membrane (GBM) antibody-mediated nephritis in rats. The experiments show that all three pretreatments exacerbate injury in this model whether judged by albuminuria or the prevalence of glomerular capillary thrombi. The effect on albuminuria was dose dependent with all three treatments. The lowest effective dose of LPS was 0.025 microgram while those for hrTNF and hrIL-1 beta were 0.4 microgram and 0.5 microgram, respectively. All three pretreatments also increased the prevalence of glomerular capillary thrombi which were rare in rats injected with anti-GBM antibodies without pretreatment. LPS pretreatment appeared to be more effective in causing glomerular capillary thrombi than hrTNF or hrIL-1 beta and this was reflected in the correlations between albuminuria and the proportion of glomeruli with capillary thrombi. This relation was linear for all three pretreatments but the slope was appreciably greater for rats pretreated with LPS (0.37) when compared with results from rats given either hrTNF (0.22) or hrIL-1 beta (0.29). Pretreatment of nephritic rats with both cytokines increased the slope to 0.42 demonstrating a synergistic effect. The synergism of hrTNF with hrIL-1 beta was also demonstrated by the effective doses needed to induce albuminuria which was evident in rats treated with 0.05 microgram of IL-1 beta and 0.4 microgram of TNF. Neither the cytokines nor LPS caused clinical, morphologic, or biochemical evidence of renal toxicity when given alone in the dose used here but they did cause a transient increase in the number of neutrophils marginated in glomerular capillaries. Pretreatment of rats with LPS or cytokines increased the glomerular neutrophil influx after anti-GBM antibodies by roughly sixfold. Our experiments show that TNF and IL-1 can increase the severity of glomerular injury in nephritis; they may be important in modulating glomerular injury clinically.
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Segal, J. "Effect of hypothyroidism on the in-vivo and in-vitro uptake of sugar by rat thymocytes and on the stimulatory response to 3,5,3′-tri-l-iodothyronine." Journal of Endocrinology 116, no. 1 (January 1988): 107–14. http://dx.doi.org/10.1677/joe.0.1160107.
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ABSTRACT We have previously demonstrated, both in vivo and in vitro, that 3,5,3′-tri-l-iodothyronine (T3) increases the uptake of the glucose analogue 2-deoxy-d-glucose (2-DG) in rat thymocytes by acting at the level of the plasma membrane. In the present study, the effect of hypothyroidism on the basal uptake of 2-DG by rat thymocytes and their response to T3 was examined. Rats were rendered hypothyroid by thyroidectomy at 21 days of age, and experiments performed with 31-and 56-day-old animals. Uptake of 2-DG by thymocytes from hypothyroid rats, both in vivo and in vitro, was greater in 31-day-old animals and less in 56-day-old animals than that in euthyroid rats. In both age-groups, hypothyroidism increased cellular responsiveness to T3, shifting the dose–response curve to the left. Similar results were obtained in experiments in which animals were rendered hypothyroid by KClO4. Injection of thyroid hormones into rats treated with KClO4 reversed the effects of hypothyroidism on uptake of [3H]2-DG by thymocytes and their response to T3. From these observations it was concluded that hypothyroidism produces a time-dependent change in basal sugar uptake by rat thymocytes, and increases cellular responsiveness to the effect of T3 at the level of the plasma membrane. J. Endocr. (1988) 116, 107–114
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Hasani, Parisa, Nargues Yasa, Sanaz Vosough-Ghanbari, Azadeh Mohammadirad, Gholamreza Dehghan, and Mohammad Abdollahi. "In vivo antioxidant potential of Teucrium polium, as compared to α-tocopherol." Acta Pharmaceutica 57, no. 1 (March 1, 2007): 123–29. http://dx.doi.org/10.2478/v10007-007-0010-z.
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In vivo antioxidant potential of Teucrium polium, as compared to α-tocopherol The present study was undertaken to explore antioxidant potential of Teucrium polium (Lamiaceae) in vivo. Antioxidant activity was measured by three tests including inhibition of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, total antioxidant power (TAP), and thiobarbituric acid reactive substances (TBARS) in serum. Rats received dry extract of T. polium in 80% ethanol by intragastric intubation at doses of 50, 100 and 200 mg kg-1 daily for 14 days. Treatment of rats with T. polium extract showed significant antioxidant activity in the DPPH test as compared to the control. T. polium extract at doses of 50 and 100 mg kg-1 significantly increased rats TAP and decreased TBARS compared to the control. Administration of T. polium at a dose of 200 mg kg-1 per day did not significantly alter serum TAP and TBARS. Antioxidant activities of T. polium at a doses of 50 and 100 mg kg-1 were in all experiments comparable to that of α-tocopherol (10 mg kg-1).
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Tyshko, N. V., and N. S. Nikitin. "INTEGRATED RESULTS OF HERMETIA ILLUCENS' PROTEIN BIOLOGICAL VALUE STUDY WITHIN IN VIVO EXPERIMENT ON 2 GENERATIONS OF RATS." BIOTECHNOLOGY: STATE OF THE ART AND PERSPECTIVES 1, no. 2022-20 (2022): 194–95. http://dx.doi.org/10.37747/2312-640x-2022-20-194-195.
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The publication presents the study results of protein biological value of black soldier fly (Hermetia illucens) larvae biomass in experiments on two generations of rats (F1 and F2) consuming the studied product during the whole period of ontogenesis.
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Trabace, Luigia, Margherita Zotti, Marilena Colaianna, Maria G. Morgese, Stefania Schiavone, Paolo Tucci, Brian H. Harvey, Gregers Wegener, and Vincenzo Cuomo. "Neurochemical differences in two rat strains exposed to social isolation rearing." Acta Neuropsychiatrica 24, no. 5 (October 2012): 286–95. http://dx.doi.org/10.1111/j.1601-5215.2011.00627.x.
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Objective: Isolation rearing of rats provides a non-pharmacological method of inducing behavioural changes in rodents that resemble schizophrenia or depression. Nevertheless, results are variable within different strains. We focused on neurochemical changes in several in vivo and post-mortem brain regions of Wistar (W) and Lister Hooded (LH) rats following post-weaning social separation.Methods: Experiments were conducted after 6–8 weeks of isolation. For post-mortem studies, prefrontal cortex (PFC), nucleus accumbens (NAC), hippocampus (Hipp) and striatum (St) were collected by tissue dissection. In vivo experiments were conducted by microdialysis in the PFC. Analyses of dopamine (DA), serotonin (5-HT) levels and relative turnover were performed by using high-performance liquid chromatography.Results: We found significant strain-related differences in biogenic amine content. LH rats were characterised by markedly raised DA, along with its turnover reduction, in all the post-mortem brain regions examined as well as in microdialysis samples, while in W rats 5-HT tissue concentration was lower in PFC and St and higher in NAC and Hipp. Cortical extracellular 5-HT concentrations were increased in group housed and decreased in isolated W animals. Moreover, isolation increased DA concentrations in the PFC of LH rats, and decreased 5-HT in W rats in NAC and Hipp. Lately, 5-HT turnover was also affected by both strain and isolation conditions.Conclusions: This study suggests that W and LH rats have markedly different neurochemical profiles in response to isolation, resulting in altered monoamine levels that vary according to brain area and rat strain. These findings highlight the importance of selecting an appropriate rat strain when considering isolation rearing to model symptoms of schizophrenia and/or depression.
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Carpinelli, Assunta, Paolo Rainone, Sara Belloli, Annalisa Reale, Andrea Cappelli, Giuliani Germano, Valentina Murtaj, et al. "Radiosynthesis and Preclinical Evaluation of 11C-VA426, a Cyclooxygenase-2 Selective Ligand." Contrast Media & Molecular Imaging 2019 (September 24, 2019): 1–12. http://dx.doi.org/10.1155/2019/5823261.
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Cyclooxygenase-2 (COX-2) is involved in the inflammatory response, and its recurrent overexpression in cancers as well as in neurodegenerative disorders has made it an important target for therapy. For this reason, noninvasive imaging of COX-2 expression may represent an important diagnostic tool. In this work, a COX-2 inhibitor analogue, VA426 [1-(4-fluorophenyl)-3-(2-methoxyethyl)-2-methyl-5-(4-(methylsulfonil)phenyl)-1H-pyrrole], was synthesized and radiolabelled with the 11C radioisotope. The ex vivo biodistribution profile of 11C-VA426 was evaluated in the brain and periphery of healthy rats and mice and in brain and periphery of inflammation models, based on the administration of LPS. 11C-VA426 synthesis with the tBuOK base showed optimal radiochemical yield (15 ± 2%) based on triflate activity, molar activity (range 37–148 GBq/μmol), and radiochemical purity (>95%). Ex vivo biodistribution studies showed a fast uptake of radioactivity but a rapid washout, except in regions expressing COX-2 (lungs, liver, and kidney) both in rats and in mice, with maximum values at 30 and 10 minutes p.i., respectively. LPS administration did not show significant effect on radioactivity accumulation. Celecoxib competition experiments performed in rats and mice treated with LPS produced a general target unrelated reduction of radioactivity concentration in all peripheral tissues and brain areas examined. Finally, in agreement with the negative results obtained from biodistribution experiments, radiometabolites analysis revealed that 11C-VA426 is highly unstable in vivo. This study indicates that the compound 11C-VA426 is not currently suitable to be used as radiopharmaceutical for PET imaging. This family of compounds needs further implementation in order to improve in vivo stability.
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Berrino, L., S. Vitagliano, S. Maione, and F. Rossi. "Glycine modulates the vascular and behavioural effects of NMDA: In vivo experiments on freely moving rats." Pharmacological Research 25 (May 1992): 105–6. http://dx.doi.org/10.1016/1043-6618(92)90310-8.
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McCully, Belinda H., Wohaib Hasan, Cole T. Streiff, Jennifer C. Houle, William R. Woodward, George D. Giraud, Virginia L. Brooks, and Beth A. Habecker. "Sympathetic cardiac hyperinnervation and atrial autonomic imbalance in diet-induced obesity promote cardiac arrhythmias." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 10 (November 15, 2013): H1530—H1537. http://dx.doi.org/10.1152/ajpheart.00196.2013.
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Obesity increases the risk of arrhythmias and sudden cardiac death, but the mechanisms are unknown. This study tested the hypothesis that obesity-induced cardiac sympathetic outgrowth and hyperinnervation promotes the development of arrhythmic events. Male Sprague-Dawley rats (250–275 g), fed a high-fat diet (33% kcal/fat), diverged into obesity-resistant (OR) and obesity-prone (OP) groups and were compared with rats fed normal chow (13% kcal/fat; CON). In vitro experiments showed that both OR and OP rats exhibited hyperinnervation of the heart and high sympathetic outgrowth compared with CON rats, even though OR rats are not obese. Despite the hyperinnervation and outgrowth, we showed that, in vivo, OR rats were less susceptible to arrhythmic events after an intravenous epinephrine challenge compared with OP rats. On examining total and stimulus-evoked neurotransmitter levels in an ex vivo system, we demonstrate that atrial acetylcholine content and release were attenuated in OP compared with OR and CON groups. OP rats also expressed elevated atrial norepinephrine content, while norepinephrine release was suppressed. These findings suggest that the consumption of a high-fat diet, even in the absence of overt obesity, stimulates sympathetic outgrowth and hyperinnervation of the heart. However, normalized cardiac parasympathetic nervous system control may protect the heart from arrhythmic events.
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Holm-Rutili, L., and K. J. Obrink. "Rat gastric mucosal microcirculation in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 248, no. 6 (June 1, 1985): G741—G746. http://dx.doi.org/10.1152/ajpgi.1985.248.6.g741.
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The superficial gastric mucosal microcirculation was observed microscopically by transillumination in the anesthetized rat. The vessels surrounding the gastric crypts were monitored on a television screen through a microscope and the pictures stored on a videotape for off-line analysis of red cell velocity (VRBC) and vessel diameter. From these measurements microvascular volume flows were calculated. VRBC reached steady values after 1-4 h (mean 2 h) and showed a regular pulsatile flow (4-7 cycles/min) in most experiments. Acid output was measured at regular intervals; 50% of the rats showed no spontaneous acid output, but the others secreted up to 100 mu eq/h. The microvessels in the superficial mucosa were classified into three orders according to their branching hierarchy and relative dimensions, and their distribution per unit mass was estimated. VRBC and volume flow were shown to decrease in the successive orders of the microvessels. Calculation of organ blood flow from microvascular flow data and vessel distribution gave values (21 ml.min-1.100 g tissue-1) that agree with earlier reported values. A higher flow velocity was detected in rats with spontaneous acid output than in those without, but there was a poor correlation between the magnitude of the acid output and VRBC. Pentagastrin (96 micrograms.kg-1.h-1) induced a significant increase in both blood flow and acid secretion. Results from this study indicate that this experimental model is potentially useful for studies of the correlation between acid secretion and mucosal blood flow.
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Fellner, Robert C., Anthony K. Cook, Paul M. O'Connor, Shali Zhang, David M. Pollock, and Edward W. Inscho. "High-salt diet blunts renal autoregulation by a reactive oxygen species-dependent mechanism." American Journal of Physiology-Renal Physiology 307, no. 1 (July 1, 2014): F33—F40. http://dx.doi.org/10.1152/ajprenal.00040.2014.
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High dietary salt is common in Western countries and is an important contributor to increased cardiovascular disease. Autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR) is an essential function of the renal microcirculation that could be affected by excessive dietary salt. High salt (HS) increases renal ROS generation partly by the enzyme NADPH oxidase. We hypothesized that a HS diet would impair autoregulation via NADPH oxidase-dependent ROS generation. The role of NADPH-dependent ROS production on the blunted autoregulatory response with a HS diet was assessed in vitro and in vivo using the blood-perfused juxtamedullary nephron preparation and anesthetized rats, respectively. The increase in renal lipid peroxidation and p67 phox expression induced by HS was prevented by apocynin treatment. Control afferent arterioles exhibited normal autoregulatory behavior in response to acute increases in renal perfusion pressure, whereas arterioles from HS rats exhibited a blunted response. Autoregulatory behavior in HS rats was restored in vitro by acute exposure to the NADPH oxidase inhibitor apocynin. At the whole kidney level, in vivo experiments showed that both RBF and GFR declined in HS rats when left kidney renal perfusion pressure was reduced from ambient to 95 mmHg, whereas control rats maintained stable GFR and RBF consistent with efficient autoregulatory behavior. Apocynin treatment improved in vivo autoregulatory behavior in HS rats and had no detectable effect in normal salt diet-fed rats. These data support the hypothesis that impaired renal autoregulatory behavior in rats fed a HS diet is mediated by NADPH oxidase-derived ROS.
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Horst, C., A. Harneit, H. J. Seitz, and H. Rokos. "3,5-Di-iodo-l-thyronine suppresses TSH in rats in vivo and in rat pituitary fragments in vitro." Journal of Endocrinology 145, no. 2 (May 1995): 291–97. http://dx.doi.org/10.1677/joe.0.1450291.
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Abstract 3,5-Di-iodo-l-thyronine (T2) is a naturally occurring metabolite of thyroxine (T4). Contrary to earlier findings, T2 has recently been shown to have rapid effects in rat liver and in mononuclear blood cells. In the experiments described here, T2 was tested to determine whether it has a TSH suppressive effect in rats in vivo and in rat pituitary fragments in vitro. In experiments over 2 weeks in rats in vivo, low doses of T2 (20–200 μg/100 g body weight per day) had no significant influence on body and organ weights, but significantly decreased TSH and T4 serum concentrations. At 200 μg/100 g per day, T2 suppressed TSH to 43% and T4 to 29% of control levels. At 1–15 μg/100 g per day, 3,5,3′-tri-iodo-l-thyronine (T3), used as a comparison to T2, had significant effects on TSH and T4 levels, and also on body weight. Fifteen μg T3/100 g per day decreased TSH to 44%, T4 to 25%, and body weight to 59% of control levels. In experiments over 3 months in rats in vivo, a low dose (25 μg/100 g per day) of T2 suppressed TSH to 60% and T4 to 57% of control levels and had no significant influence on other parameters. Conversely, 0·1 μg/100 g per day T3 had significant effects on body and organ weights as well as pellet intake, but a less pronounced TSH suppressive effect: TSH concentrations were unchanged and T4 concentrations were down to 80% of control values. In rat pituitary fragments in vitro, a clear suppression of TSH secretion after a TRH pulse was demonstrated. To summarise, T2 is a specific agonist in the negative feedback mechanism on TSH secretion at the pituitary level without other apparent thyromimetic effects. Journal of Endocrinology (1995) 145, 291–297
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Antonioli, Luca, Carolina Pellegrini, Matteo Fornai, Laura Benvenuti, Vanessa D’Antongiovanni, Rocchina Colucci, Lorenzo Bertani, et al. "Preclinical Development of FA5, a Novel AMP-Activated Protein Kinase (AMPK) Activator as an Innovative Drug for the Management of Bowel Inflammation." International Journal of Molecular Sciences 22, no. 12 (June 13, 2021): 6325. http://dx.doi.org/10.3390/ijms22126325.
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Acadesine (ACA), a pharmacological activator of AMP-activated protein kinase (AMPK), showed a promising beneficial effect in a mouse model of colitis, indicating this drug as an alternative tool to manage IBDs. However, ACA displays some pharmacodynamic limitations precluding its therapeutical applications. Our study was aimed at evaluating the in vitro and in vivo effects of FA-5 (a novel direct AMPK activator synthesized in our laboratories) in an experimental model of colitis in rats. A set of experiments evaluated the ability of FA5 to activate AMPK and to compare the efficacy of FA5 with ACA in an experimental model of colitis. The effects of FA-5, ACA, or dexamethasone were tested in rats with 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis to assess systemic and tissue inflammatory parameters. In in vitro experiments, FA5 induced phosphorylation, and thus the activation, of AMPK, contextually to the activation of SIRT-1. In vivo, FA5 counteracted the increase in spleen weight, improved the colon length, ameliorated macroscopic damage score, and reduced TNF and MDA tissue levels in DNBS-treated rats. Of note, FA-5 displayed an increased anti-inflammatory efficacy as compared with ACA. The novel AMPK activator FA-5 displays an improved anti-inflammatory efficacy representing a promising pharmacological tool against bowel inflammation.
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Tanzer, J. M., L. Grant, A. Thompson, L. Li, J. D. Rogers, E. M. Haase, and F. A. Scannapieco. "Amylase-binding proteins A (AbpA) and B (AbpB) differentially affect colonization of rats' teeth by Streptococcus gordonii." Microbiology 149, no. 9 (September 1, 2003): 2653–60. http://dx.doi.org/10.1099/mic.0.26022-0.
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Streptococcus gordonii produces two α-amylase-binding proteins, AbpA and AbpB, that have been extensively studied in vitro. Little is known, however, about their significance in oral colonization and cariogenicity (virulence). To clarify these issues, weanling specific pathogen-free Osborne-Mendel rats, TAN : SPFOM(OM)BR, were inoculated either with wild-type strains FAS4-S or Challis-S or with strains having isogenic mutations of abpA, abpB, or both, to compare their colonization abilities and persistence on the teeth. Experiments were done with rats fed a sucrose-rich diet containing low amounts of starch or containing only starch. The mutants and wild-types were quantified in vivo and carious lesions were scored. In 11 experiments, S. gordonii was a prolific colonizer of the teeth when rats were fed the sucrose (with low starch)-supplemented diet, often dominating the flora. Sucrose-fed rats had several-fold higher recoveries of inoculants than those eating the sucrose-free, starch-supplemented diet, regardless of inoculant type. The strain defective in AbpB could not colonize teeth of starch-only-eating rats, but could colonize rats if sucrose was added to the diet. Strains defective in AbpA surprisingly colonized better than their wild-types. A double mutant deficient in both AbpA and AbpB (abpA/abpB) colonized like its wild-type. Wild-types FAS4-S and Challis-S had no more than marginal cariogenicity. Notably, in the absence of AbpA, cariogenicity was slightly augmented. Both the rescue of colonization by the AbpB− mutant and the augmentation of colonization by AbpA− mutant in the presence of dietary sucrose suggested additional amylase-binding protein interactions relevant to colonization. Glucosyltransferase activity was greater in mutants defective in abpA and modestly increased in the abpB mutant. It was concluded that AbpB is required for colonization of teeth of starch-eating rats and its deletion is partially masked if rats eat a sucrose-starch diet. AbpA appears to inhibit colonization of the plaque biofilm in vivo. This unexpected effect in vivo may be associated with interaction of AbpA with glucosyltransferase or with other colonization factors of these cells. These data illustrate that the complex nature of the oral environment may not be adequately modelled by in vitro systems.
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Liang, Qiang, Xiaoran Li, Wangning Zhou, Yu Su, Shenbao He, Shuanglei Cheng, Jianzhong Lu, et al. "An Explanation of the Underlying Mechanisms for the In Vitro and In Vivo Antiurolithic Activity of Glechoma longituba." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/3134919.
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Purpose. To use in vitro and in vivo models to evaluate Glechoma longituba extract to provide scientific evidence for this extract’s antiurolithic activity. Materials and Methods. Potassium citrate was used as a positive control group. Oxidative stress (OS) markers and the expression of osteopontin (OPN) and kidney injury molecule-1 (KIM-1) were measured to assess the protective effects of Glechoma longituba. Multiple urolithiasis-related biochemical parameters were evaluated in urine and serum. Kidneys were harvested for histological examination and the assessment of crystal deposits. Results. In vitro and in vivo experiments demonstrated that treatment with Glechoma longituba extract significantly decreased calcium oxalate- (CaOx-) induced OPN expression, KIM-1 expression, and OS compared with the positive control group (P<0.05). Additionally, in vivo rats that received Glechoma longituba extract exhibited significantly decreased CaOx deposits and pathological alterations (P<0.05) compared with urolithic rats. Significantly lower levels of oxalate, creatinine, and urea and increased citrate levels were observed among rats that received Glechoma longituba (P<0.05) compared with urolithic rats. Conclusion. Glechoma longituba has antiurolithic effects due to its possible combined effects of increasing antioxidant levels, decreasing urinary stone-forming constituents and urolithiasis-related protein expression, and elevating urinary citrate levels.
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Pinzariu, Alin Constantin, Teodor Oboroceanu, Florin Zugun Eloae, Ioana Hristov, Victor Vlad Costan, Luminita Labusca, Petru Cianga, et al. "Vitamin D as a Regulator of Adipocyte Differentiation Effects in vivo and in vitro." Revista de Chimie 69, no. 3 (April 15, 2018): 731–34. http://dx.doi.org/10.37358/rc.18.3.6187.
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The age-associated adiposity and the effect of long-term vitamin D was studied in vitamin D deficient rats. In in vivo experiments, the influence of a 9 months of vitamin D treatment (weekly oral gavage with 0.125 mg vitamin D3 (5000 IU)/100g body weight) on the adipocyte precursors from the omental adipose tissue was examinated. In in vitro experiment, rat adipose-derived mesenchymal stromal/stem cells (ASCs) were induced to differentiate into adipocytes in the presence or absence of 25(OH)D3 (0.25, 25, and 2500 nmol/L). ASCs derived from vitamin D-treated animals showed an increase adipogenic potential as compared to vitamin D-deficient rats. The addition of 25(OH)D3 inhibits the adipocyte differentiation and lipid deposition in a dose dependent manner.