The effect of banazepril on the expressions of TGFβ 1 and its receptor in diabetic rat kidney cortex

AIM To investigate the effect of benazepril on the expressions of TGFβ 1 and its receptor (TβR) in diabetic rat kidney cortex. METHODS The rats were randomly divided into following groups: uninephrectomized (group C), streptozotocin diabetic rats (group D) and diabetic rats treated with benazepril (10 mg·kg -1 ·d -1 , by gavage, group DB). Blood glucose, serum insulin, serum creatinine lever and body weight, kidney weight as well as renal protein protein content were observed after 4 weeks of treatment. ACE activities were measured by spectrofluorimetry in plasma, renal cortex and medulla. mRNA expressions of TGFβ 1, 1α(IV) precollagen and FN were determined by Northern blot; protein expressions of TGFβ 1 and TβRⅠ was measured by Western blot in renal cortex. RESULTS After 4 weeks of treatment, benazepril could significantly ameliorate hyperglycemia, decreased serum insulin, elevated serum creatinine and body weight loss, kidney hypertrophy. Northern blot showed the expressions of TGFβ 1, 1α(IV) precollagen, FN mRNA were increased by 3 94, 4 25 and 1 50 folds, respectively; Western blot showed the expressions of TGFβ 1 amd TβRⅠ were elevated by 3 10 and 1 10 folds. However, benazepril could significantly suppress their expressions. In addition, there was an increase in renal cortex ACE activities despite a decrease in plasma ACE activities. Administration of benazepril could reduce ACE activities in plasma and renal cortex by approximately 92 00%, 88 77%, respectively. CONCLUSION Benazepril could significantly suppress the expressions of TGFβ 1 and its receptor, These might be its main mechanism of nephroprotection in diabetic model.