Objective: This study aims to investigate the role and mechanism of 1, 25-dihydroxyvitamin D3 in type 2 diabetic nephropathy rats.
Methods: There were 30 male Sprague-Dawley (SD) rats that were randomly divided into 3 groups: the normal control group (NC group, n=10), the diabetic nephropathy model group (T2DN model group, n=10), and the diabetic nephropathy group treated with 1, 25-dihydroxyvitamin D3 (vD3-T2DN group, n=10). After 15 weeks, the changes of renal tissues morphology, renal function, and 24 h urinary protein quantification were measured. The expressions of Transforming Growth Factor beta 1 (TGF-β1), CD68 and Monocyte Chemoattractant Protein-1 (MCP-1) in renal cortex were also detected by Immunohistochemistry (IHC).
Results: The weight of rats were significantly decreased in T2DN model group and vD3-T2DN group than in NC group (P<0.05) at the end of 15th week, while the blood glucose, 24 h urinary protein and triglyceride were significantly increased (P<0.01). The expression of TGF-β1, CD68 and MCP-1 in T2DN model group and vD3-T2DN group were significantly higher than in NC group (P<0.01). Compared with NC group, the triglyceride (P<0.01) and serum creatinine (P<0.05) were significantly higher in T2DN model group. In vD3-T2DN group, the expression of TGF-β1, CD68 and MCP-1, the content of 24 h urinary protein (P<0.01), and triglyceride (P<0.05) were significantly than in T2DN model group.
Conclusion: Through repressing the expression of TGF-β1, CD68 and MCP-1, 1, 25-dihydroxyvitamin D3 can inhibit invasion of macrophages to protect kidney of T2DN rats.