Spermidine alleviating oxidative stress and apoptosis by inducing autophagy of granulosa cells in Sichuan white geese

Spermidine have been reported a role in antioxidative, antiaging, and antiinflammatory. Oxida-tive stress causes granulosa cell (GC) apoptosis, follicu-lar atresia, and impairs poultry reproductive functions. Studies have found that autophagy is the protective mechanism against antioxidant stress and apoptosis in cells. However, the relationship between spermidine-induced autophagy, oxidative stress, and apoptosis in goose GCs remains unclear. In this study, we investi-gated the autophagy mechanism to mediate spermidine effects on the alleviation of oxidative stress and apopto-sis in goose GCs. Follicular GCs were treated with sper-midine combination with 3-Nitropropanoic acid (3-NPA), rapamycin (RAPA), and chloroquine (CQ) or with hydrogen peroxide, RAPA, and CQ. Spermidine upregulated the ratio of LC3-II/I, inhibited the accu-mulation of p62 protein, and induced autophagy. 3-NPA treatment significantly increased ROS produc-tion, MDA content, SOD activity, cleaved CASPASE-3 protein expression, and decreased BCL-2 protein expression in follicular GCs. Spermidine inhibited oxi-dative stress and apoptosis induced by 3-NPA. In addi-tion, hydrogen peroxide-induced oxidative stress was inhibited by spermidine. However, the inhibitory effect of spermidine was eliminated under chloroquine. Our results demonstrated that spermidine relieved oxidative stress and apoptosis of GCs by inducing autophagy, indicating that spermidine has a great potential to maintain proteostasis and sustain granulosa cell viability in geese.