Quercetin Alleviates Endoplasmic Reticulum Stress-Induced Apoptosis in Buffalo Ovarian Granulosa Cells

Simple Summary Granulosa cells are critical components of the ovary that nurture germ cells and sustain oocyte maturation. Apoptosis of granulosa cells leads to follicular atresia, which in turn leads to female infertility. There are many reasons for the apoptosis of granulosa cells, one of which is apoptosis induced by endoplasmic reticulum stress. We found that quercetin could attenuate the effects of endoplasmic reticulum stress on granulosa cells by the PERK/CHOP signaling pathway. The results provide a novel strategy for inhibiting the apoptosis of granulosa cells. Endoplasmic reticulum (ER) stress plays a crucial role in granulosa cell (GCs) apoptosis, which is the main cause of follicular atresia. Quercetin (QC), a plant-derived flavonoid, has antioxidant, anti-inflammatory, and other biological properties. However, whether QC can alleviate the effects of ER stress on buffalo GCs remains unknown. In this study, we constructed an ER stress model in buffalo GCs by using tunicamycin (TM) and pre-treated with QC to explore the effect of QC on cells under ER stress. Apoptosis was detected by Annexin fluorescein 5 isothiocyanate (V-FITC), and the expressions of mRNA and related proteins involved in ER stress and apoptosis were detected via real-time polymerase chain reaction and Western blot. The results revealed that ER stress can cause apoptosis in GCs, whereas QC pre-treatment can prevent apoptosis caused by ER stress. After pre-treatment with QC, the expression levels of ER stress-related genes and proteins significantly decreased, pro-apoptotic genes were significantly down-regulated, and anti-apoptotic genes were significantly up-regulated. Furthermore, the results of Chop gene overexpression suggested that QC alleviated ER stress via the PERK/CHOP signaling pathway. In this study, we preliminarily elucidated that QC alleviates ER stress-induced apoptosis in buffalo GCs, and the results suggest a novel strategy for delaying follicular atresia by inhibiting GCs apoptosis.