The Roles Of AR And TGF-β₁ In The Pathogenesy Of Rat's Polycystic Ovarian Syndrome

Polycystic ovarian syndrome (PCOS), mainly featuring the androgen excess and the chronic anovulation, is one of the most common endocrine disorder diseases among the women of childbearing ages. The incidency rate accounts for 5%—21% among the infertility women and 75%-80% among the anovulatory women. In 1935, Stein and Leventhal initially reported a group of syndrome principally characterizing amenorrhea, obesity, hirsutism, anovulation and the bilateral ovarian polycystic changes. Due to the very extensive changes of physiopathology which involves in genetics, neuroendocrinology, glycometabolism, adipic-metabolism, protein-metabolism and the abnormality of partial regulating and controlling factors of ovary, its research is still remained one of the hotspots in Gynecological endocrinology field by now. PCOS mainly characterizes androgen excess along with chronic anovulatory. Hypersecretion of androgen in ovary is the key reason to result in the PCOS. It is crucial to understand the androgen excess—the characteristics changes in ovary, for elucidate polycystic ovary syndrome pathogenesis. In previous reports, it has been suggested that PCOS is likely to be a result of the cytokines regulator disorder.The cytokine of transforming growth factor β 1 (TGF- β 1)has multiful functionsfor regulating growth and differentiation, inhibiting inflammation and immunity. TGF-β1 in ovary is produced by the ovary through self-secreation and sied-secreation. Different size of follicles have different leval of TGF-β...