Objective To study the role of TGF-β1 in the formation of interstitial fibrosis and capsular thickening in the PCOS rats. Methods PCOS rat model were established by subcutaneous injection DHEA. Estradiol (E2), testosterone (T), follicular stimulating hormone (FSH), luteinizing hormone (LH), LH/FSH and fasting insulin (FINS) hormone values of the model were tested by microparticle enzyme immunoassay, the pathohistology of PCOS rat ovaries was observed by HE staining, and their ultrastructure was tested by transmission electron microscope (TEM). The expressions of TGF-β1 in PCOS group (n=20), and control group(n=20) were detected and evaluated by immunohistochemistry and image analysis system. Results The results of serum E2, T, LH/FSH, FINS, the ovarian pathological-histology and the ultrastructure showed 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 developing 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 cause of capsular thickening and interstitial fibrosis. TGF-β1 also takes part in regulating PCOS follicle development and atresia. Objective To study the role of TGF-β1 in the formation of interstitial fibrosis and capsular thickening in the PCOS rats. Methods PCOS rat models were established by subcutaneous injection DHEA. Estradiol (E2), testosterone (T), follicular stimulating hormone , Luteinizing hormone (LH), LH / FSH and fasting insulin (FINS) hormone values ​​of the model were tested by microparticle enzyme immunoassay, the pathohistology of PCOS rat ovaries was observed by HE staining, and their ultrastructure was tested by transmission electron microscope ( Results of TGF-β1 in PCOS group (n = 20), and control group (n = 20) were detected and evaluated by immunohistochemistry and image analysis system. Results The results of serum E2, T, LH / FSH, FINS, the ovarian pathological-histology and the ultrastructure showed 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 diffe (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 cause of capsular thickening and interstitial fibrosis. TGF-β1 also takes part in regulating PCOS follicle development and atresia.