Objective: To investigate the mechanism of valsartan in protecting the renal lesion of diabetic rats.
Methods: The following groups of rats were studied: normal control rats, streptozotocin diabetic rats and diabetic rats treated with valsartan (8 mg x kg(-1) x d(-1)). Mean arterial pressure, plasma glucose, serum insulin, serum creatinine, urinary albumin, ACE activity and Ang II concentration of kidney as well as profile of kidney hypertrophy were observed after 2, 4, 8 weeks of treatment, while TGF beta(1) mRNA expression of kidney cortex was assessed by Northern blot analysis, TGF beta(1), fibronectin and collagen IV expression were measured by immunohistochemistry.
Results: Serum creatinine level (P < 0.05), urinary albumin excretion and kidney hypertrophy index (P < 0.01) of valsartan treated group were significantly lower than those of diabetic untreated group. There was a significant increase in mRNA expression of TGF beta(1) and protein expression of of TGF beta(1) fibronectin and collagen IV in diabetic rats (P < 0.01). The expression of TGF beta(1) mRNA and protein (P < 0.01) as well as the protein expression of fibronectin and collagen IV (P < 0.05) in the valsartan group were much lower than that in the diabetic group.
Conclusion: The results suggested that valsartan has some renal protective effect on diabetes in rats, partly through down-regulating TGF beta(1) expression and reducing deposition of glomerular ECM.