RESUMO
This study aimed to evaluate the therapeutic role of erythropoietin (EPO) or myoinositol versus metformin (MET) in improving the reproductive functions and glucose tolerance in a rat model of polycystic ovary (PCOS). Oral letrozole (LTZ) was used for induction of PCOS in wester rats for 21 days, after that, MET, EPO and myoinositol were administered for the following 21 days. The LTZ-induced PCOS rats have lost their oestrous cyclicity and become fixed at the diestrus phase, developed insulin resistance, abnormal sex and gonadotrophin hormone serum levels, increased cystic follicles, decreased number of the growing follicles and very little or no corpora lutea on microscopic examination, which were reversed by the three drugs, MET, EPO and myoinositol. MET and myoinositol were mostly equally effective in improving the reproductive manifestations of the disease. However, EPO was most effective in decreasing the insulin level observed in this LTZ-induced model of PCOS.
RESUMO
BACKGROUND: Tobacco use is responsible for millions of preventable deaths due to cancer. Nicotine, an alkaloid chemical found in tobacco was proved to cause chronic inflammation and oxidative stress. The transcription factor STAT1 induces the expression of many proinflammatory genes and has been suggested to be a target for anti-inflammatory therapeutics. The following study investigated the effect of Nicotine on STAT1 pathway and oxidative stress in rat lung tissue. METHODS: Thirty rats were divided into 3 groups; group I considered as control, group II; its rats were daily injected with Nicotine at a dose of 0.4 mg/100 gm body for 8 successive weeks and group III; its rats were daily injected with Nicotine as group II, but the injection was stopped for another 4 weeks. STAT1α protein was assessed by immunohistochemistry, COX-2 and iNOS genes expression were evaluated by real time PCR and thiobarbituric acid reactive substances (TBARS) and total thiols were measured using spectrophotometric methods in the lung tissues of the rats. RESULTS: The results of the study revealed that group II rats had the highest expression of STAT1α protein and COX-2 and iNOS genes and oxidative stress in their lung tissues. Nicotine cessation for 4 weeks caused a marked reduction in the expression of STAT1α protein, COX-2 and iNOS genes and oxidative stress. CONCLUSION: Induction of STAT1 pathway and the increase in oxidative stress may be the mechanisms through which Nicotine may induce its harmful effects.
