Dioscin Ameliorates Polycystic Ovary Syndrome by Inhibiting PI3K/Akt Pathway-Mediated Proliferation and Apoptosis of Ovarian Granulosa Cells

Abstract

To understand the mechanism underlying Dioscin inhibition of polycystic ovary syndrome, we have examined its effects on ovarian granulosa cells from letrozole-treated rats. To this end, Western blot was utilized to determine changes in the levels of Bcl-2, cleaved caspase-3, caspase-3, and phosphatidylinositol 3-kinase (PI3K)/protein kinase B pathway after Dioscin treatment in letrozole-treated rats. Dioscin ameliorated polycystic ovary syndrome by reducing the serum level of testosterone and increasing progesterone levels. It also inhibited proliferation and induced apoptosis of ovarian granulosa cells in the rat model by decreasing the level of Bcl-2 and elevating cleaved caspase-3. Western blot analysis revealed that Dioscin suppressed the PI3K/Akt pathway by inhibiting p-AKT/AKT. SC79, a p-AKT/AKT activator, reversed the effects of Dioscin on the proliferation and apoptosis of ovarian granulosa cells. In conclusion, Dioscin might present a novel therapeutic opportunity for patients with polycystic ovary syndrome.