Abstract
A significant decrease in poultry egg production occurs due to ovarian aging and autophagy is one of the important factors of ovarian aging that is induced predominantly by oxidative stress. Increasing evidence showed potential roles of plant-derived grape seed proanthocyanidin (GSPs) in protecting ovarian granulosa cells (GCs) from oxidative damage, although the underlying mechanism is still unclear. Here we investigated the possible functions of autophagy involved in the preventive effect of GSPs on oxidative stress in the GCs of ovarian hierarchical follicles of laying chickens. The results showed that increased autophagy was observed in the aging hens (580-day-old, D580) compared with the peak-lay hens (D280). Treatment of GSPs significantly restored the elevated autophagy and decreased viability of cultured D280 chicken GCs that were elicited by hydrogen peroxide. GSPs also suppressed the increased autophagy in the natural aging hens. Similar to the effect of GSPs on GC viability, inhibition of autophagy also showed a protective effect on the decreased viability of GCs under oxidative damage. However, GSPs were not able to provide further protection in GCs that were pretreated with 3-methyladenine (an autophagy inhibitor). In addition to its promoting action on antioxidant capacity, treatment with GSPs increased survival of GCs from autophagy that was caused by oxidative stress through the FoxO1-related pathway. Inhibition of FoxO1 or activation of PI3K-Akt pathway by GSPs increased the confrontation of GCs to oxidative damage and decreased autophagy in GCs. In addition, activation of the SIRT1 signal inhibited the GCs autophagy that was caused by oxidative stress via GSPs-induced deacetylation of FoxO1. These results revealed a new mechanism of GSPs against oxidative stress of GCs via inhibiting FoxO1, which was probably a possible target for alleviating ovarian aging in laying poultry.
Highlights
The egg production of the commercial laying chicken decreases around 580 days (D580) and this decrease seriously affects the economic output of laying poultry
Activation of the Silent information regulator of transcription 1 (SIRT1) signal inhibited the granulosa cells (GCs) autophagy that was caused by oxidative stress via grape seed proanthocyanidins (GSPs)-induced deacetylation of FoxO1. These results revealed a new mechanism of GSPs against oxidative stress of GCs via inhibiting FoxO1, which was probably a possible target for alleviating ovarian aging in laying poultry
The results of Hematoxylin and eosin (H&E) and immunofluorescence assay showed that the formation of autophagy was remarkably enhanced in ovaries and follicles collected from D580 hens as compared with D280 hens (Figures 1A–D)
Summary
The egg production of the commercial laying chicken decreases around 580 days (D580) and this decrease seriously affects the economic output of laying poultry. Ovarian follicles represent the most important functional unit for the continuation of the avian species and egg production. There are increasing atretic follicles in the aging hens and follicular atresia in poultry is similar to that in mammals, which is mainly due to apoptosis of granulosa cells (GCs) (Matsuda-Minehata et al, 2006). Oxidative stress, which is caused by the accumulation of reactive oxygen species (ROS) in metabolic activities, signifies one of the most important factors leading to ovarian aging (Devine et al, 2001; Luderer, 2014; Lim et al, 2015). Elucidation of the preventive mechanism of GC death caused by oxidative stress may provide a potential treatment strategy for reproductive failure caused by excessive follicular atresia
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