卡托普利对糖尿病大鼠肾脏保护机制的研究

Study of renal protective mechanism of Captopril in diabetic rats

目的 研究卡托普利对糖尿病大鼠肾脏病变的保护作用及其机制。方法 应用卡托普利对糖尿病大鼠治疗12周 ,观察大鼠肾脏结构和功能、血丙二醛 (MDA)、肾组织中 NO、糖基化终末产物 (AGEs)、环磷腺苷 (c AMP)、转化生长因子β1 (TGFβ1 )的改变。结果 卡托普利治疗后能明显降低血肌酐、2 4小时尿蛋白 ,阻止肾脏肥大和肾小球硬化 ,并降低 MDA、TGFβ1 、AGEs含量 ,升高 NO、c AMP含量。结论 卡托普利通过抗脂质过氧化、抑制肾 AGEs生成和 TGFβ1 表达 ,升高肾脏 NO、c

Objective To sutdy the protective mechenism of Captopril on the kidney of diabetic rats.Methods Male Sprague-Dawley rats,rendered to be diabetic with streptozocin (STZ),were treated with captopril dissolved in dringing water for 12 weeks.The serum creatinine,blood urea nitrigen (BUN),proteinuria,blood malondialdehyde(MDA),and the content of NO,cAMP,and advanced glycosylation end products (AGEs) in renal tissue were measured.The renal pathological lesions and the expression of TGFβ 1 were also investigated.Results Captopril supplementation reduced the serum creatinine and proteinuria.The abnormal changes in kidney morphology were ameliorated.The blood MDA,the expression of TGFβ 1 and the content of AGEs in the test group were significantly lower than controlled diabetic rats,the renal NO and cAMP were enhanced.Conclusion Administration of Captopril to rats with STZ-diabeties could ameliorate diabetic nephropathy.This beneficial effect could be related to reduced oxidant injury,less accumulation of AGEs,inhibition of the expression of TGFβ 1,and enhance renal NO and cAMP.