1,25-dihydroxyvitamin D3 alleviates bisphenol A-induced apoptosis in KGN cells by improving mitochondrial activity and blocking the mitochondrial cytochrome c apoptotic pathway

Abstract

Abstract Purpose This study explored whether and how 1,25-dihydroxyvitamin D3 (1,25(OH)2VD3) mitigates bisphenol A (BPA)-induced apoptosis in human ovarian granulosa KGN cells to obtain a theoretical basis for how vitamin D improves ovarian function in patients with polycystic ovary syndrome (PCOS). Methods The effect of different concentrations of BPA and 1,25(OH)2VD3 on KGN cell viability was clarified. Then, KGN cells were treated with BPA to induce apoptosis and subsequently exposed to 1,25(OH)2VD3. The apoptosis rate, reactive oxygen species (ROS) level, and mitochondrial function of the cells were assessed as well as the expression levels of genes related to apoptosis, antioxidant pathways, and mitochondrial biogenesis. Results BPA dose-dependently inhibited the proliferation and viability of the KGN cells, induced a significant increase in oxidative stress and apoptosis, and disrupted mitochondrial function. The expression levels of apoptotic genes in the mitochondrial cytochrome c (Cyt c) pathway were upregulated, and those of antioxidant and mitochondrial biogenesis genes were downregulated. 1,25(OH)2VD3 significantly ameliorated apoptosis and mitochondrial damage. Conclusions 1,25(OH)2VD3 reduces BPA-induced KGN cell damage and apoptosis by improving mitochondrial activity and blocking the mitochondrial Cyt c apoptotic pathway. This indicates that the vitamin D levels in PCOS patients of childbearing age should be monitored.