Quercetin protects the survival and decidualization of endometrial stromal cells in PCOS mice by enhancing autophagy through PI3K/Akt/FoxO1

Polycystic ovary syndrome (PCOS) can lead to increased abortion rates. Quercetin treats PCOS, but its specific mechanism has not been fully clarified. PCOS was induced in mice by dehydroepiandrosterone, and decidualization was induced by corn oil. Mice were treated with quercetin, autophagy inhibitor 3-MA, autophagy inducer rapamycin, PI3K inhibitor LY294002, and PI3K inducer 740Y-P. Pathological damage in the ovary and uterus was observed by HE staining. The levels of sex hormones, metabolism, and inflammatory factors were detected using ELISA. The survival and decidualization of endometrial stromal cells were identified by immunohistochemistry, immunofluorescence, qRT-PCR, and Western blot. Autophagy and the PI3K/Akt/FoxO1 pathway-related protein levels were detected by Western blot. The theca cell layer and endometrium of PCOS mice were significantly thinner. The levels of sex hormone, pro-inflammatory factors, COX-2, integrin ???3, and autophagy-related proteins were obviously raised, while Vimentin, IGFBP-1, PRL, and PI3K/Akt/FoxO1 pathway expression were significantly decreased. The above indices were reversed considerably after quercetin treatment. 3-MA could reduce the level of autophagy, LY294002 could reduce the levels of PI3K/Akt/FoxO1 pathway, Vimentin, and PRL, and increase the level of autophagy. In conclusion, quercetin enhanced autophagy through the PI3K/Akt/FoxO1 pathway; thereby protecting endometrial stromal cells and improving decidualization disorders.