Protective effects of ginsenosides against Bisphenol A-induced cytotoxicity in 15P-1 Sertoli cells via extracellular signal-regulated kinase 1/2 signalling and antioxidant mechanisms.

Numerous studies have demonstrated that Bisphenol A (BPA) can cause reproductive toxicity. Ginseng has wide range of pharmacological actions and, more importantly, has proven its worth with respect to reproductive function in several reports. We have suggested that ginsenosides, the main active components of ginseng, may protect against BPA-induced cell damage. Therefore, an in vitro culture model of 15P-1 Sertoli cells was employed to investigate whether ginsenosides have protective effects on BPA-stimulated 15P-1 Sertoli cells. The results revealed that ginsenosides (75 μg/ml) significantly inhibited BPA-induced decreases in cell viability and increases in apoptosis. Immunofluorescence staining showed that BPA exposure-induced collapse of vimentin intermediate filaments was prevented by the application of ginsenosides. Ginsenosides also inhibited extracellular signal-regulated kinase (ERK1/2) phosphorylation and BPA-induced alterations of Bcl-2 and Bax protein expression in 15P-1 Sertoli cells. Furthermore, the alterations of T-AOC, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione and malondialdehyde levels in BPA-stimulated cells were partially prevented with pre-treatment with ginsenosides. Taken together, these results suggest that ginsenosides have protective effects against BPA-induced cell damage and that these effects are mediated by preventing ERK1/2 phosphorylation and through the enhancement of cellular antioxidant capacity. Ginsenosides may therefore be beneficial in the prevention of environmental BPA-induced, reproduction-related toxicity.