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Increased follicular atresia occurs with aging and results in reduced fecundity in laying chickens. Therefore, relieving follicular atresia of aging poultry is a crucial measure to maintain sustained high laying performance. As an antiaging agent, metformin was reported to play important roles in preventing aging in diverse animals. In this study, the physiological state of the prehierarchical follicles in the peak-laying hens (D280) and aged hens (D580) was compared, followed with exploration for the possible capacity of metformin in delaying atresia of the prehierarchical follicles in the aged D580 hens. Results showed that the capacity of yolk deposition within follicles declined with aging, and the point of endoplasmic reticulum- (ER-) mitochondrion contact decreased in the ultrastructure of the follicular cells. Meanwhile, the expression of apoptosis signaling genes was increased in the atretic small white follicles. Subsequently, the H2O2-induced follicular atresia model was established to evaluate the enhancing capacity of metformin on yolk deposition and inhibition of apoptosis in the atretic small white follicles. Metformin inhibited apoptosis through regulating cooperation of the mitochondrion-associated ER membranes and the insulin (PI3K/AKT) signaling pathway. Furthermore, metformin regulated calcium ion homeostasis to relieve ER-stress and inhibited release of mitochondrion apoptosis factors (BAD and caspase). Additionally, metformin activated PI3K/AKT that suppressed activation of BAD (downstream of the insulin signaling pathway) in the atretic follicles. Further, serum estrogen level and liver estrogen receptor-α expression were increased after dietary metformin supplementation in D580 hens. These results indicated that administration of dietary metformin activated the PI3K/AKT and calcium signaling pathway and enhanced yolk deposition to prevent chicken follicular atresia.

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The increase in follicular atresia and the decrease in the fecundity of laying hens occur with the aging process. Therefore, the key measure for maintaining high laying performance is to alleviate follicular atresia in the aging poultry. Follicle-stimulating hormone (FSH), as an important pituitary hormone to promote follicle development and maturation, plays an important role in preventing reproductive aging in diverse animals. In this study, the physiological state of the prehierarchical small white follicles (SWFs) and atretic SWFs (ASWFs) were compared, followed by an exploration of the possible capacity of FSH to delay ASWFs’ progression in the hens. The results showed that the DNA damage within follicles increased with aging, along with Golgi complex disintegration, cell cycle arrest, increased apoptosis and autophagy in the ASWFs. Subsequently, the ACNU-induced follicular atresia model was established to evaluate the enhancing capacity of FSH on increasing cell proliferation and attenuating apoptosis in ASWFs. FSH inhibited DNA damage and promoted DNA repair by regulating the CHK2/p53 pathway. Furthermore, FSH inhibited CHK2/p53, thus, suppressing the disintegration of the Golgi complex, cell cycle arrest, and increased autophagy in the atretic follicles. Moreover, these effects from FSH treatment in ACNU-induced granulosa cells were similar to the treatment by a DNA repair agent AV-153. These results indicate that FSH protects aging-resulted DNA damage in granulosa cells by inhibiting CHK2/p53 in chicken prehierarchical follicles.