Literature DB >> 26097534

Protective effects of calcitriol on diabetic nephropathy are mediated by down regulation of TGF-β1 and CIP4 in diabetic nephropathy rat.

Rui Yu1, Jiangfeng Mao2, Ye Yang1, Yuanyuan Zhang1, Yanyan Tian1, Jun Zhu1.   

Abstract

OBJECTIVE: To explore the protective effects of calcitriol on diabetic nephropathy by modulating the expressions of transforming growth factor-beta 1 (TGF-β1) and Cdc42 interacting protein-4 (CIP4).
METHODS: Streptozotocin-induced diabetic nephropathy rats (n=36) were randomly divided into control group (control-H, control-M, control-L) and calcitriol group (calcitriol-H, calcitriol-M, calcitriol-L). The expression of TGF-β1 gradually decreased in control-H, control-M and control-L subgroups by injection of different virus vectors. Peanut oil and calcitriol were given to control and calcitriol group, respectively. The expressions of TGF-β1 and CIP4 in kidney, the pathology, and the renal function and lipid profiles were compared between control and calcitriol treatment groups.
RESULTS: In the control group, the higher level of TGF-β1 was associated with more severe glomerular pathology (P<0.05). There is a positive correlation between the expression of CIP4 and TGF-β1. Control-H subgroup had significant more severe kidney disease, higher levels of cholesterol, triglyceride, blood glucose, blood urea nitrogen (BUN) and creatinine (Cr) than control-M and control-L subgroups. After calcitriol treatment, the expression of TGF-β1 and CIP4 were significantly decreased compared to the corresponding control subgroups (all P<0.05). Renal fibrosis and pathological changes were markedly improved. The levels of cholesterol, triglyceride, blood glucose, BUN and Cr were significantly reduced (P<0.05).
CONCLUSION: Calcitriol may protect diabetic nephropathy from fibrosis via inhibition of TGF-β1 and CIP4.

Entities:  

Keywords:  Cdc42 interacting protein-4 (CIP4); Diabetic nephropathy; calcitriol; transforming growth factor beta 1 (TGF-β1)

Mesh:

Substances:

Year:  2015        PMID: 26097534      PMCID: PMC4466921     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


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