TGF-β_1在PCOS卵巢间质纤维化形成中的作用

目的:探讨TGF-β1在PCOS大鼠卵巢间质纤维化、包膜硬化形成中的作用。方法:利用脱氢表雄酮(DHEA)皮下注射的方法建立PCOS病理模型大鼠20只,用微粒子酶免分析法测定血清性激素E2、T、LH、FSH、LH/FSH、空腹胰岛素(FINS)水平,及光镜下观察PCOS大鼠卵巢的病理结构,透射电镜观察细胞超微结构来验证模型。采用免疫组化法检测PCOS组(n=20)卵巢细胞因子TGF-β1的表达,并与20只正常大鼠相比照。结果:TGF-β1在PCOS组各阶段卵泡卵母细胞、颗粒细胞的表达强度与对照组相比,差异无统计学意义(P>0.05)。而在窦状卵泡膜细胞和卵巢间质细胞中的表达,PCOS组显著高于对照组(P<0.01,P<0.05)。结论:多囊卵巢中TGF-β1表达异常,可能是导致多囊卵巢间质纤维化、包膜增厚的原因之一,TGF-β1也参与PCOS卵泡发育、闭锁的调控。

Role of TGF-β1 in the Formation of Ovarian Interstitial Fibrosis in PCoS Rat

Objective:To explore the local role of TGF-β1 in the PCOS rats in the formation of interstitial fibrosis, capsular thickening. Methods:PCOS rat model was established by subcutaneous injection DHEA. E2, T, FSH, LH, LH/FSH and fasting insulin (FINS) hormone values of the model were tested by microparticle enzyme immunoassay, the pathohistology of PCOS rats' ovarian structure was observed by HE staining. The expressions of TGF-β1 protein in PCOS group (n=20), and control group (n=20) were detected and evaluated by immunohistochem-istry and image analysis system. Results:The results of serum E2, T, LH/FSH, FINS, and the pathological-histology, the ultrastructure of ovary show that the model was established successfully. Compared with control group, there was no significant difference of TGF-β1 expression intensity in oocytes, granulosa cells of the different developmental stages of follicle in PCOS (P>0.05). But it was markedly higher expressed in the theca cells of antral follicles (P<0.01), and stromal cells (P<0.05) in PCOS group than in control group. Conclusion:The abnormal expression of TGF-β1 in PCOS is the main causes of capsular thickening, interstitial fibrosis. TGF-β1 also takes part in regulating PCOS follicle development and atresia.