Selenium Protects Follicular Granulosa Cells from Apoptosis Induced by Mercury Through Inhibition of ATF6/CHOP Pathway in Laying Hens

The purpose of this research was to explore the effect of selenium on mercury-mediated apoptosis of follicular granulosa cells in laying hens. Moreover, the ATF6/CHOP pathway was investigated to explore the mechanism in this progress. Hg, Se, and 4-phenyl butyric acid were used alone or in combination to treat the cells. Our results showed that the nuclear in cells became condensate after Hg exposure, while Se addition significantly alleviated this change. Hg exposure significantly induced the apoptosis and the reduction of mitochondrial membrane potential in cells ( P < 0.05). Nevertheless, co-treatment of Se significantly inhibited these effects ( P < 0.05). Additionally, Hg exposure dramatically elevated the gene expressions of Bax/Bcl-2 ( P < 0.05), caspase-3 ( P < 0.05), caspase-9 ( P < 0.05), protein kinase RNA-like endoplasmic reticulum kinase ( P < 0.05), activating transcription factor 6 ( P < 0.05), C/EBP homologous protein (CHOP; P < 0.05), inositol-requiring enzyme 1α ( P < 0.05), tumor necrosis factor-associated factor 2 ( P < 0.05), activating transcription factor 6 (ATF6; P < 0.05), and apoptosis signal-regulating kinase 1 ( P < 0.05) in cells, whereas Se addition avoided these changes. The exposure to Hg considerably boosted the expression of ATF6 and CHOP protein ( P < 0.05), while Se addition significantly alleviated the above-mentioned enhancements ( P < 0.05). In summary, Hg exposure induced apoptosis, which was considerably reduced alleviated by Se addition, which was linked to the ATF6/CHOP pathway in follicular granulosa cells in laying hens.