卡托普利对糖尿病肾病大鼠血浆同型半胱氨酸和肾功能的影响

目的：探讨卡托普利对糖尿病肾病（ DN）大鼠血浆同型半胱氨酸（ homocystiene，Hcy）和肾功能的影响及其作用机制。方法采用链脲佐菌素（strepotozotocin，STZ）诱导 SD 大鼠建立糖尿病模型30只，随机分为空白对照组、DN 组、卡托普利组3组，每组10只。卡托普利组以17.5 mg /（kg·d）卡托普利灌胃，空白对照组、DN 组以等量生理盐水灌胃，1/ d。于干预后12周末检测各组大鼠血浆 Hcy 含量、肾组织血管紧张素Ⅱ（ angiotensin Ⅱ，AngⅡ）含量、尿素、肌酐、尿白蛋白排泄率（ urinary albumin excretion rate，UAER）、肾重/体重，采用实时聚合酶链反应（ real-time PCR）检测肾组织蛋白激酶 C（protein kinase C，PKC）及其亚型 PKCα的 mRNA 相对表达水平。结果与空白对照组比较，DN 组 Hcy 含量、AngⅡ含量、尿素、肌酐、UAER、肾重/体重、PKC 及其亚型 PKCα的 mRNA 相对表达水平显著升高（P ﹤0.05）；与 DN 组比较，卡托普利组以上指标显著降低（ P ﹤0.05）。结论卡托普利可降低 DN 大鼠 Hcy 的表达水平并有效保护其肾功能，其机制可能为通过抑制肾脏 PKCα信号激活而发挥作用。

Effect of Captopril on Plasmic Homocysteine and Renal Function in Rats with Diabetic Nephropathy

Objective To investigate the effect of Captopril on plasmic homocysteine(Hcy)and renal function in rats with diabetic nephropathy(DN)and its mechanism. Methods The diabetes mellitus models were established in 30 Sprague Dawley(SD)rats with Streptozotocin(STZ),and were randomly divided into control group,DN group and Captopril group(n = 10 for each group). Captopril group was lavaged with 17. 5 mg /( kg·d)Captopril(1 / d),while the control and DN groups were lavaged with same volume of physiological saline(1 / d). In all groups,contents of plas-ma Hcy and angiotensin Ⅱ(AngⅡ)in nephridial tissue,levels of urea and creatinine,urinary albumin excretion rate (UAER)and kidney weight / body weight were detected,relative expression levels of mRNA in protein kinase C(PKC) and isoforms PKCα in nephridial tissue were detected using real-time polymerase chain reaction(PCR)after 12 weeks of treatment. Results Compared with those in control group,the values of Hcy and AngⅡ contents,levels of urea and creatinine,UAER,kidney weight / body weight,relative expressions of mRNA in PKC and PKCα were significantly in-creased in DN group(P ﹤ 0. 05). Compared with those in DN group,the above values were significantly decreased in Captopril group(P ﹤ 0. 05). Conclusion Captopril may decrease level of Hcy expression and protect renal function of diabetic nephropathy rats,and its mechanism may exert its effect by inhibiting PKCα signal activation.