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| AngⅡ抑制剂对HIF-1α在慢性肾衰大鼠肾组织中表达的影响 |
| 秦军燕1,王琛1,2*,杨婧1,邵命海1,留寅清1,何立群1,2 |
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(1. 上海中医药大学附属曙光医院肾病科,上海 200021;
2. 上海市中医临床重点实验室, 上海 200021
*通信作者) |
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| 摘要: |
| 目的观察AngⅡ抑制剂对于5/6(ablation/infarction,A/I) 肾切除慢性肾衰大鼠残余肾组织HIF-1α蛋白及mRNA表达的影响,并初步探讨其作用机制。方法将SD雄性大鼠随机抽取15只设为假手术组(A组),其余采用5/6(A/I) 肾切除慢性肾衰模型法制作成慢性肾功能衰竭动物模型,随机分为模型组(B组)和AngⅡ抑制剂(氯沙坦钾合福辛普利钠)组(C组),每组15只，分别给予相应干预,60 d后检测生化指标,并采用蛋白质印迹法和荧光定量PCR分别测定大鼠残余肾皮质、髓质HIF-1α蛋白及mRNA的表达。结果模型组与假手术组比较,SCr、BUN升高, CCr降低(P均<0.01);AngⅡ抑制剂组与模型组干预后比较，SCr、BUN水平下降,CCr水平升高(P均<0.05)。模型组大鼠肾皮质、髓质HIF-1α蛋白和mRNA的表达均较假手术组升高(P<0.05),AngⅡ抑制剂组HIF-1α蛋白和mRNA在肾皮质和髓质中的表达均较模型组减少(P<0.05)。结论AngⅡ抑制剂可以改善5/6(A/I)肾切除慢性肾衰大鼠的肾功能,其作用机制可能与HIF-1α信号通路有关。 |
| 关键词: 缺氧诱导因子1,α亚基 肾纤维化 肾功能衰竭 血管紧张素Ⅱ 缺氧 |
| DOI：10.3724/SP.J.1008.2012.00965 |
| 投稿时间：2012-04-08修订日期：2012-06-18 |
| 基金项目:国家自然科学基金(30973723), 上海市科委基金(08411962400), 上海高校创新团队建设基金资助项目(201203). |
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| Effects of angiotensin Ⅱ inhibitor on HIF-1α expression in the renal tissue of 5/6th kidney ablation/infarction rats |
| QIN Jun-yan1,WANG Chen1,2*,YANG Jing1,SHAO Ming-hai1,LIU Yin-qing1,HE Li-qun1,2 |
(1. Department of Nephrology, Shuguang Hospital, Shanghai University of TCM, Shanghai 200021, China;
2. Shanghai Key Clinical Laboratory of TCM, Shanghai 200021, China
*Corresponding author.) |
| Abstract: |
| ObjectiveTo investigate the influences of Angiotensin Ⅱ inhibitor on renal expression of HIF-1α mRNA and protein in the chronic renal failure (CRF) rats (induced by 5/6th kidney ablation/infarction \[5/6A/I\]) and the related mechanism. MethodsSD rats were made into CRF model by means of 5/6th kidney ablation/infarction. The study was divided into sham operation group (Group A), model group (Group B) and Angiotensin Ⅱ inhibitor(Cozaar-with-Monopril) group (Group C), each group containing 15 rats. The biochemical parameters of the rats were examined 60 days later in the 3 groups. The expression of HIF-1α mRNA and protein in the remnant renal cortex and medulla were assessed by Real-time PCR and Western blotting analysis. ResultsCompared with group A, group B had significantly increased SCr and BUN levels and significantly decreased CCr level(P<0.01). Compared with group B, group C had significantly decreased SCr and BUN levels and significantly increased CCr level(P<0.05). The expression of HIF-1α mRNA and protein in the renal cortex and medulla in group B was significantly higher than that in group A(P<0.05), and that in group C was significantly lower than that in group B (P<0.05). ConclusionAngiotensin Ⅱ inhibitor can improve the renal function in CRF rats induced by 5/6(A/I), which might be associated with HIF-1α signaling pathway. |
| Key words: hypoxia-inducible factor 1, alpha subunit renal fibrosis kidney failure angiotensin Ⅱ anoxia |
