Gallic acid regulates autophagy to alleviate hydrogen peroxide-induced oxidative damage in granulosa cells

Autophagy is closely related to the development of the ovaries. Gallic acid (GA) exhibits various biological activities, including antioxidant, anti-inflammatory, and potential regulatory effects, on autophagy. However, the relationship of GA with autophagy and oxidative damage in granulosa cells (GCs) has not been elucidated. This study aimed to investigate the role of GA in alleviating hydrogen peroxide (H ₂ O ₂ )-induced oxidative damage in GCs via autophagy regulation.Herein, cell viability, oxidative stress (OS), inflammatory markers and reproductive-related hormones were measured to evaluate the effects of GA. Notably, GA alleviated H ₂ O ₂ -induced decrease in GC viability. Reactive oxygen species, malondialdehyde, tumor necrosis factor-α, interleukin (IL)-6, and IL-1β were all markedly increased in GCs after H ₂ O ₂ treatment. Moreover, this treatment reduced the levels of superoxide dismutase, catalase, total antioxidant capacity and reproductive-related hormone. After the H ₂ O ₂ treatment, terminal deoxynucleotidyl transferase dUTP nick end labeling staining demonstrated a significant rise in cell death. However, GA treatment inhibited H ₂ O ₂ -induced oxidative damage, inflammation, and apoptosis. Western blotting analysis for evaluating the effect of GA on autophagy by detecting autophagy-related protein levels and related pathways revealed that GA reduced the H ₂ O ₂ -induced increase in autophagy. Altogether, the results of this study show that GA alleviates OS and cell death in GCs by regulating autophagy, Therefore, from the standpoint of autophagy control, GA might contribute to ovarian damage prevention.