Effects of vitamin D on pancreatic islet β cell injury induced by low concentration cadmium in mice

Abstract

The aim of this study was to investigate the effect of Vitamin D on pancreatic islet β cell injury induced by low concentration cadmium in mice. The islet β cell line NIT-1 cells were divided into normal control group, Cdcl2 group and Cdcl2+vitamin D3 (VD) group. Cell viability was detected by CCK-8 assay. Insulin content in the supernatant was detected by enzyme-linked immunoassay (ELISA). Reactive oxygen species (ROS) content was detected by flow cytometry, and changes of insulin-related genes were detected by real-time fluorescence quantitative PCR. Changes of insulin receptor substrate-1 (IRS-1) and insulin receptor substrate-2 (IRS-2) were detected by Western blotting. The results showed that the concentration of Cdcl2 (0.05 mM) which had no significant effect on the viability of NIT-1 cells was screened by CCK-8 method, where the concentration of active vitamin D (1 nM) for the cytotoxicity induced by a low concentration of cadmium could be reduced. The insulin secretion ability of NIT-1 cells was detected. The results showed that under 4-day exposure to a low concentration of cadmium, the insulin secretion of NIT-1 cells increased at first (P<0.05), and then decreased with the prolongation of cadmium exposure (P<0.05). The intervention of active vitamin D eventually increased the insulin secretion of the cadmium-exposed cells (P<0.05). At the gene expression level, long-term exposure of a low concentration of cadmium did not significantly change the expression of insulin gene, but significantly increased the ROS content in NIT-1 cells (P<0.05), while the ROS content in NIT-1 cells was decreased by the intervention of active vitamin D (P<0.05). In conclusion, the insulin secretion of islet β cells increased at the early stage of long-term low concentration cadmium exposure, and then decreased with the prolongation of cadmium exposure. This effect was affected by active vitamin D intervention.