Supplemenation of selenium attenuates cisplatin induced podocyte injury via BCL-2/BAX/ caspase-3 pathway

Selenium (Se) is an essential trace element and micronutrient primarily discovered in selenoproteins, and involves in the regulation of redox and antioxidant cytoprotection through the glutathione- and the thioredoxin-dependent redox, and therefore this study aims to elucidate the prevention of Se on the cisplatin induced podocyte damage, and further explores its potential mechanism. To address it, murine podocyte cells-5 was selected and treated with gradient cisplatin, including 7.5 mu g/ml, 15 mu g/ml and 30 mu g/ml, and the cell proliferation activity, the expression level of methane dicarboxylic aldehyde (MDA), glutathione peroxidase (GSH-Px) and glutathione (GSH), the cell apoptosis level was determined to validate the optimal concentration. Based on it, after Se treatment, the cell proliferation activity, the expression level of MDA, GSH-Px and GSH, and the protein expression level of apoptosis associated proteins, including B-cell lymphoma-2 (Bcl-2), Bcl-2 Associated X (Bax) and Caspase-3 was examined. As expected, when different dosages of cisplatin were added, both cell survival rate and GSH expression level were significantly decreased, and the expression level of MDA and GSH-Px and the cell apoptosis level were significantly increased, the results also showed that 15 mu g/ml of cisplatin was the optimal concentration. However, after Se treatment, both cell survival rate and GSH expression level were significantly increased when compared to that of cisplatin-treated group, and the expression level of MDA, GSH-Px and the cell apoptosis were significantly decreased when compared to that of cisplatin-treated group. In addition, the level of protein expression of BCL-2 was significantly decreased after cisplatin treatment, but was significantly increased after Se treatment, similarly, that of BAX and Caspase-3 was significantly increased after cisplatin treatment, and was significantly decreased after Se treatment, these indicated that cisplatin had a significant cytotoxicity, and Se could reduce the cytotoxicity of cisplatin via the decrease of oxidative stress and cell apoptosis level, these exhibited a significant application value in clinic.