Vitamin D3 Ameliorates High Glucose-Induced Podocyte Apoptosis

Abstract

Objective: Diabetic kidney disease (DKD) is a severe kidney disease characterized by podocyte apoptosis, injury, and accumulation of extracellular matrices that ultimately lead to end-stage renal disease. Vitamin D3 was reported to provide renal protection in DKD through the Vitamin D receptor (VDR), however there was limited data on whether it has a protective effect on podocytes of DKD induced by high glucose. Methods: The experimental subjects were conditionally immortalized mouse podocytes (MPC-5), which were divided into 4 groups: NG (normal glucose) group, HM (Hypertonic) group, HG (high glucose) group, VD3 (HG +1,25-dihydroxyvitamin D3 (1,25-D3)) group. Western-blot analysis was performed to detect the expression of Bcl-2, Bax and Caspase-3 in podocytes. The mRNA Expression of Bcl-2, Bax and Caspase-3 in the three groups were detected by RT-PCR method. Results: Compared with the NG group, the expression of apoptosis proteins Caspase-3 and Bax in the podocytes of HG group increased, and the expression of Bcl-2 decreased. Pretreatment with vitamin D3 attenuated these abnormalities in podocytes in HG group. Conclusion: Vitamin D can alleviate the apoptosis of podocytes induced by high glucose in vitro.