Résumé
Type I diabetes mellitus results from the autoimmune destruction of the p cells in pancreatic islets. Currently, extensive research is being conducted on the generation of insulin-producing cells [IPCs] from stem cells. P19 embryonal carcinoma cells are multipotent and can differentiate into cell types of all three germ layers. In this study, the differentiation of P19 cells into IPCs by using mouse pancreas extract [MPE] was investigated. Embryoid bodies [EBs] obtained from P19 cells were cultured in medium containing 3% fetal bovine serum, supplemented by concentration of 50, 100, 200,300 pg/mL MPE for 7-14 days. Dithizone [DTZ] staining was used to detect IPCs derived from EBs in vitro. Mouse monoclonal insulin-proinsulin and monoclonal insulin receptor beta antibodies were used for immunoflourescence. Insulin content from the cells and insulin secreted by differentiated cells in response to concentrations of 5.5 and 25 mM glucose were measured using ELISA kits. DTZ-positive cells showed purple-red clusters, immunoflourescence indicated expression of Beta cell markers [insulin-proinsulin and insulin receptor beta] in these cells. Increasing glucose concentration, caused more insulin to be secreted by differentiated ceils. P19 cells can in the presence of pancreas extract differentiate to cell producing and secreting insulin cells. Differentiated cells can increase insulin secretion in response to increasing glucose medium
Résumé
Oxidative stress is caused by the imbalance between production of pro-oxidants and the antioxidant defenses. Reactive oxygen species [ROS] can play an important role in the pathogenesis of cardiovascular diseases. The present study aimed at investigating whether administration of oxytocin ameliorates oxidative stress induced by experimental myocardial infarction in rats. Cardiac ischemia-reperfusion [I/R] was induced by occlusion of left main coronary artery of rats for 25 min, followed by a period of reperfusion for 2h. OT at doses of 0.0001-1 microg was administered intraperitoneally 30 min prior to ischemia. Following reperfusion, blood samples were taken for measuring the plasma MDA levels, as an index of lipid peroxidation. We observed a dose-dependent association between dose of oxytocin and plasma MDA. Oxytocin 0.01microg significantly reduced MDA levels as compared to control group. Blockade of specific OT receptors by atosiban attenuated the anti-oxidative effect of OT. The MDA level in the L-NAME and atropine groups were higher than those in the OT group and reach to control group, whereas the MDA levels in the anantin group were same as OT group and significantly lower than those in the control group. Oxytocin has a beneficial effect, mediated by NO and Ach, on cardiac tissue against oxidative damage due to I/R, suggesting that oxytocin can be used to tissue protection against oxidative stress