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.
Highlights
Diabetic kidney disease (DKD) is part of the most common chronic complications of diabetes mellitus, which can lead to end-stage renal disease (ESRD) with clinical manifestation of progressively worsening albuminuria and a declining glomerular filtration rate[1]
The decrease of Bcl-2/Bax induces the activation of Caspase and the apoptosis of downstream cells, which plays an important role in the regulation of apoptosis
Our results showed that 1,25-D3 can improves the expression of Bcl-2/Bax and Caspase-3 in podocyte apoptosis in a high glucose environment
Summary
DKD is part of the most common chronic complications of diabetes mellitus, which can lead to end-stage renal disease (ESRD) with clinical manifestation of progressively worsening albuminuria and a declining glomerular filtration rate[1]. There is increasing evidence that podocyte apoptosis is an important determinant of proteinuria and glomerular sclerosis in diabetic patients[5,6]. High glucose induces podocyte apoptosis through the activation and regulation of Bax, BCL2 and Caspase[3 7]. The vitamin D endocrine system was believed to play an important role in bone metabolism, calcium homeostasis and contribute to cell differentiation, cell growth inhibition and immune regulation[8]. A recent clinical trial shows that paricalcitol, an activated vitamin D analog, can reduce proteinuria in DKD patients. A recent clinical trial shows that paricalcitol, an activated vitamin D analog, can reduce proteinuria in DKD patients10. 1,25-D3 prevents puromycin aminonucleoside from apoptosis of glomerular podocytes by activating the Phosphatidylinositol
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
