| Objective Investigate the effect of rosiglitazone on reproductive hormone, glucose tolerance abnormality, ovarian morphology and ovarian granulose cell apoptosis of polycystic ovary syndrome (PCOS) rat model induced by dehydroepiandrosterone (DHEA), to explore the potential link between insulin resistance (IR) and ovarian granulose cell apoptosis in the etiology of PCOS, and supply the evidence of effective clinical therapy of rosiglitazone.Method Selected 44 average 23-day-old immature female SD rats and randomly divided them into 4 groups. One group was controlled, and the other three groups were to be PCOS rat models. After completing the PCOS rat models, all the rats were performed oral glucose tolerance test (OGTT). The total PCOS rats were again divided into PCOS1 group, PCOS2 group and rosiglitazone group according to the level of 2hPG of OGTT. Drew blood and got ovaries from the rats of controlled and PCOS1 group under the condition of narcotization. After the rats of PCOS2 and rosiglitazone group respectively administrate water for injection and rosiglitazone for 4 weeks, so did they as the former. All the rats were examined and compared the levels of serum fast insulin (FIN), follicle stimulate hormone (FSH), luteinizing hormone (LH), testosterone (T), estradiolum (E2), progesterone (P), and prolactin (PRL) with radioimmunoassay(RIA). The ovaries of each group rats underwent fixing, dewatering, paraffin imbedding, microtome section, and then observed their morphology under the HE stain condition by light microscope, and the ovarian granulose cell apoptosis by electron microscope. In addition, compared the apoptosis incident of the granulose cells by TUNEL assay among them. All the results were put into multiple comparison.Result The levels of 2hPG, FIN, and T elevated significantly in the PCOS1 group compared with those in the controlled group (P<0.05) .The levels of LH and LH/FSH also elevated, but their differences were not significant. It's worth noting that the increase of the levels of LH in PCOS2 group differ significantly with PCOS1 group ( P<0.01). The levels of LH, T, 2hPG, FIN in rosiglitazone group decreased significantly compared with PCOS2 group (P<0.05). In contrast, the levels of P in rosiglitazone group elevated significantly compared with PCOS2 group (P<0.01). The results of ovarian HE stain revealed that there were some corepus luteum, various stage follicles, and the development of dominant follicles in controlled group; Ovaries were obviously cystic, and there were a few corepus lutem in PCOS1 group and PCOS2 group. There were a large number of corepus luterm in rosiglitazone group. Observed by electron microscope that granulose cell morphous was normal in controlled group and rosiglitazone group, but it's evidently apoptotic in PCOS1 group and PCOS2 group. Apoptotic incident (AI) with apoptotic cell TUNEL in situ assay decreased significantly in rosiglitazone group compared with PCOS2 group (P<0.05 ) .conclusion1 The reduced-dehydroepiandrosterone PCOS rats are characteristic with hyperandrogenism, polycystic ovary (PCO) morphology and insulin resistance (IR). When completing the model, they do not reverse, but worsen. So the PCOS rat model can well imitate the feature of PCOS patient. 2 PCOS rats are typical of granulose cell apoptosis.3 Rosiglitazone can alter hyperandrogenism and hyperluteinizing hormonism, restrain insulin resistant and hyperinsulinism and prevent granulose cell apoptosis in PCOS rats. Moreover, it can promote ovulation and it is a kind of affective medicine to cure PCOS.4 We can infer that rosiglitazone can reduce granulose cell apoptosis by means of restraining insulin resistance. Insulin resistance and granulose cell apoptosis are two aspect of pathogenesis in PCOS, and they influence each other.
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