Effect of ACE inhibitor on early kidney hypertrophy and its mechanism in diabetic rats
- VernacularTitle:CE抑制剂对糖尿病大鼠早期肾脏肥大的抑制作用及机制
- Author:
Yonggui WU
;
Shanyan LIN
;
- Publication Type:Journal Article
- Keywords:
diabetic nephropathy;
ACE inhibitor;
kidney hypertrophy;
p21 CIP1 protein
- From:
Chinese Pharmacological Bulletin
1987;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM To explore the effect of ACE inhibitor on early kidney hypertrophy and its mechanism in diabetic rats. METHODS Rats were randomly divided into three groups: uninephrectomized rats, streptozotocin induced diabetic rats and diabetic rats treated with benazepril (an ACE inhibitor, 10 mg?kg -1 ?d -1 , ig). Activity of ACE was determined by the fluorimetric assay. Expression of TGF? 1 mRNA and TGF? 1 and p21 CIP1 protein was measured by Northern blot analysis and Western blot analysis, respectively. RESULTS After 1 week, the diabetic rats developed a body weight loss, kidney weight/body weight increased and renal cortex ACE activity elevated despite a decrease in plasma ACE activity. Northern blot analysis showed that renal cortex TGF? 1 mRNA expression in the diabetic rats was enhanced by 1.3 times, compared with uninephrectomized rats. Western blot analysis showed that TGF? 1 and p21 CIP1 protein expression were also increased. Administration of benazepril for one week significantly suppressed kidney hypertrophy. ACE activity in the plasma, renal cortex and medulla was reduced by 89%,70% and 70 5%, respectively. Expression of TGF? 1 mRNA as well as expression of TGF? 1 and p21 CIP1 protein was reduced by 47 7%, 49 5% and 60 0%, respectively. CONCLUSION Our results suggest that the suppression of ACE inhibitor on diabetic kidney hypertrophy might partially be associated with a decrease in the expression of TGF? 1 and p21 CIP1 in diabetic rats renal cortex. However, its exact mechanism remains to be further explored.
