肾衰Ⅱ号方对慢性肾功能衰竭大鼠肾组织AngⅡ及nNOS蛋白表达的影响

作者	单位
秦军燕	上海中医药大学附属曙光医院肾病科
王琛	上海中医药大学上海市教委创新团队,肝肾疾病病证教
邵命海	上海中医药大学上海市教委创新团队,肝肾疾病病证教
杨婧	上海中医药大学上海市教委创新团队,肝肾疾病病证教
李睿琳	上海中医药大学上海市教委创新团队,肝肾疾病病证教

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中文摘要:

目的观察肾衰Ⅱ号方对5/6(ablation/infarction,A/I)肾切除慢性肾功能衰竭(chronic renal failure,CRF)大鼠残余肾组织纤维化及血管紧张素Ⅱ(AngⅡ)和神经型一氧化氮合酶(nNOS)表达的影响,并初步探讨其作用机制。方法选取57只SD雄性大鼠按5/6(A/I)肾衰模型法制备大鼠模型。造模后随机分为模型组、肾衰Ⅱ号方组(中药组,肾衰Ⅱ号方浓煎液2mL灌胃)和西药组(氯沙坦钾合福辛普利钠混悬液,2mL灌胃),每组15只,另选取15只大鼠作为正常组,正常组和模型组予等量纯净水灌胃,各组均每天干预1次,连续干预60天。检测各组大鼠SCr、BUN、内生肌酐清除率(creatinine clearance rate,CCr),采用Western blot法测定大鼠残余肾皮质、髓质AngⅡ和nNOS蛋白表达,观察肾组织病理形态。结果与正常组比较,模型组SCr、BUN升高,CCr降低(P<0.01),提示造模成功。与本组干预前比较,中药组及西药组SCr、BUN水平下降,CCr水平升高(P<0.01)。与模型组比较,中药组及西药组SCr、BUN水平及髓质AngⅡ表达均降低(P<0.01,P<0.05),CCr水平及皮质、髓质nNOS表达明显升高(P<0.01,P<0.05)。肾组织病理显示,中药组病理变化明显减轻,优于模型组。结论肾衰Ⅱ号方可以改善5/6肾切除CRF大鼠的肾功能,减轻肾间质纤维化,其作用机制可能与调节肾内失衡的AngⅡ和nNOS信号转导途径有关。

英文摘要:

Objective To observe the effects of Shenshuai Ⅱ Recipe(SSR) on the fibrosis of remnant nephridial tissue and expressions of Ang Ⅱ and nNOS in the chronic renal failure(CRF) rats induced by 5/6 ablation/infarction(A/I),and to preliminarily investigate its mechanism of action.Methods Fifty-seven SD male rats were used to prepare the CRF rat model by means of 5/6 A/I.After modeling,they were randomly divided into the model group,the SSR group(2 mL SSR condensed decoction given by gastrogavage),and the Western medicine group(treated by 2 mL suspension of losartan potassium and fosinopril sodium given by gastrogavage),15 rats in each group.Another 15 rats were recruited as the normal control group.Equal volume of pure water was given to rats in the normal control group and the model group.Relevant treatment was given to rats in each group once daily,for 60 successive days.The serum creatinine(SCr),blood urea nitrogen(BUN),and creatinine clearance rate(CCr) were detected.The expressions of angiotensin Ⅱ(Ang Ⅱ) and nervous system type nitric oxide synthase(nNOS) in the remnant renal cortex and the medulla were detected by Western blot.The pathomorphology of the nephridial tissue was observed.Results Compared with the normal control group,the levels of SCr and BUN increased(P<0.01) and the level of CCr decreased(P<0.01) in the model group,indicating a successful modeling.Compared with the same group before treatment,the levels of SCr and BUN decreased and the level of CCr increased in the SSR group and the Western medicine group(all P<0.01).Compared with the model group after treatment,the levels of SCr and BUN decreased,and the expression of Ang Ⅱ in the medulla decreased in the SSR group and the Western medicine group(P<0.01,P<0.05).The levels of CCr and protein expressions of nNOS in the renal cortex and the medulla obviously increased in the SSR group and the Western medicine group(P<0.01,P<0.05).The pathology of the nephridial tissue showed that the pathological changes in the SSR group were obviously ameliorated,better than those of the model group.Conclusions SSR could improve the renal function and relieve the renal interstitial fibrosis in the rats induced by 5/6 A/I.Its mechanism of action was possibly correlated with regulating the renal imbalanced Ang Ⅱ and nNOS signal transduction pathway.

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