Effects of valsartan on expression of nitric oxide and transforming growth factor-β1 in the glomeruli of diabetic rats
Ding-Wu Zhang
Abstract
Ding-Wu Zhang
Abstract
Objective:To investigate the effect of angiotensin receptor antagonist Valsartan on the level of nitric oxide (NO) and the expression of and transforming growth factor-β1 (TGFβ1) in renal cortex of diabetic rats. Methods :Diabetic rats were induced by intraperitoneal Streptozotocin injection (60mg/kg) at one dose. The 24 rats were randomly divided into 3 groups: normal control group(NC), diabetic model group(DM) and Vasartan-treated diabetic group (Val). At the end of 12 weeks, body weight, creatinine, uria nitrogen, glucose level of plasma and 24 urinary albumin excretion were detected. NO level in serum and renal tissue was measured. The protein expression of TGFβ1 in renal cortinal was examined by immunohistochemistry. Results: After 12 weeks, the level of serum creatinine and proteinuria in group Val were significantly lower than those in DM group (P0.05). NO level of serum and renal tissue were significantly decreased in Val group compared with those of DM group. Vasartan therapy significantly reduced the expression of renal TGF-β1 in diabetic rats compared with controls. The positive integrated intensity was reduced by about 79.2% in Val group. The pathological changes under light microscopy in Val group were less obvious than that in DM group. Conclusion: Valsartan may have kidney protective effect on diabetic rats, partly through increasing NO level of renal tissue and suppresing the overexpression of TGF-β1, thus decreasing the excretion of urinary albumin and improving the glomerular matrix accumulation and preventing the progression of diabetic nephropathy.
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Objective:To investigate the effect of angiotensin receptor antagonist Valsartan on the level of nitric oxide (NO) and the expression of and transforming growth factor-β1 (TGFβ1) in renal cortex of diabetic rats. Methods :Diabetic rats were induced by intraperitoneal Streptozotocin injection (60mg/kg) at one dose. The 24 rats were randomly divided into 3 groups: normal control group(NC), diabetic model group(DM) and Vasartan-treated diabetic group (Val). At the end of 12 weeks, body weight, creatinine, uria nitrogen, glucose level of plasma and 24 urinary albumin excretion were detected. NO level in serum and renal tissue was measured. The protein expression of TGFβ1 in renal cortinal was examined by immunohistochemistry. Results: After 12 weeks, the level of serum creatinine and proteinuria in group Val were significantly lower than those in DM group (P0.05). NO level of serum and renal tissue were significantly decreased in Val group compared with those of DM group. Vasartan therapy significantly reduced the expression of renal TGF-β1 in diabetic rats compared with controls. The positive integrated intensity was reduced by about 79.2% in Val group. The pathological changes under light microscopy in Val group were less obvious than that in DM group. Conclusion: Valsartan may have kidney protective effect on diabetic rats, partly through increasing NO level of renal tissue and suppresing the overexpression of TGF-β1, thus decreasing the excretion of urinary albumin and improving the glomerular matrix accumulation and preventing the progression of diabetic nephropathy.
Key concepts: Medicine, Diabetic nephropathy, Internal medicine, Endocrinology, Valsartan, Streptozotocin, Creatinine, Renal cortex