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.

Objective To investigate the expression of transforming growth factor ?_1(TGF?_1)in renal cortex from uninephrectomized diabetic rats. Methods Wistar rats were divided into uninephrectomized rats(group A), streptozotocin diabetic rat(group B). Blood glucose, serum insulin level and body weight, kidney weight, kidney weight/body weight as well as renal tissue protein contents were observed after 1, 4 weeks of streptozotocin injection. The expression of TGF?_1, precollagen 1?(Ⅳ) and fibronectin mRNA were measured by Northern blot analysis, and TGF?_1 protein by Western blot analysis in kidney cortex. In addition, ACE activities were determined by fluorimetric assay in plasma, kidney cortex and medulla. Results Group B demonstrated significantly elevated blood glucose and decreased serum insulin level. Kidney weight、kidney weight/body weight and renal tissue protein contents progressively increased despite total body weight loss. There was significant(P

AIM: To study effect of benazepril (an ACE inhibitor) on expression of insulin receptor (IR) and its substrate-1(IRS-1) protein in renal tissue cell membrane in diabetic rats. METHODS: The rats were randomly divided into following groups: control (n=6), streptozotocin induced diabetic (n=7) and diabetic treated with benazepril (n=7). Body weight, kidney weight and kidney weight/body weight were observed after 4 weeks of treatment. ACE activities in plasma, renal tissue were measured by the fluorimetric assay. The expressions of IR and IRS-1 protein were determined by Western blot analysis in renal tissue cell membrane. RESULTS: After 4 weeks of treatment, benazepril significantly ameliorated kidney hypertrophy in diabetic rats. ACE activities in plasma, renal tissue were redunced by approximately 92.00% and 88.77%, respectively. Western blot analysis showed that the expressions of IR and IRS-1 protein were increased by 2.1 and 1.5 folds in renal tissue cell membrane in diabetic rats. However, benazepril reduced expression of IR and IRS-1 protein by 45.74% and 47.66%, respectively. CONCLUSIONS: Increased expression of IR and IRS-1 protein might be related to abnormally active glucose metabolism in diabetic rat kidney. Down-regulation of expression of IR and IRS-1 protein might be one of important machnisms of Benazepril nephroprotection on diabetic rats.

Uninephrectomy was performed in a ll rats of this study, and diabetic model was induced in partial rats by streptozo tocin. Then these rats were divided into uninephrectomy group, diabetes group an d benazepril-treated diabetes group. After 4 weeks, renal tubulo-interstitial morphological change was observed and type Ⅳ collagen, fibronectin and transfor ming growth factor ? 1 (TGF-? 1) proteins as well as TGF-? 1 mRNA were d etermined. The results suggested that benazepril played a protective role in ren al tubulo-interstitial injury, which was associated partially with down-regula ted overexpression of TGF-? 1.

Objective: To evaluate the feasibility and effect of transcatheter closure of ventricular septal defects(VSD) using the VSD occluder.Methods: From December 2003 to March 2005,13 VSD patients,8 males and 5 females,ranging in age from 4 to 35(15.2?10.7)years,underwent catheter closure using the VSD occluder.Tthe mean diameter of the VSD obtained by transthoracic echocardiography was 4-12(5.4?1.2) mm.Transcatheter closure was performed under transthoracic echocardiographic guidance after left ventriculography.All patients were followed up 1,3 and 6 months after the procedures. Results: The devices were successfully placed in 12 of the patients and complete closure achieved in 11.Trace residual shunt was observed in 1 patient but disappeared within 10 minutes.No severe complications were noted except 1 case of complete right bundle branch block revealed by electrocardiography. Conclusion: Transcatheter closure of VSD by the VSD occluder is a safe and effective procedure,with good immediate results.Further clinical trials are under way to assess its long-term effect.