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中国临床药理学与治疗学 ›› 2008, Vol. 13 ›› Issue (9): 1002-1004.

• 基础研究 • 上一篇    下一篇

缬沙坦对自发性高血压大鼠肾脏核因子-κB 蛋白表达的影响

杨玉雯, 王德国, 孔祥权, 徐承华   

  1. 皖南医学院附属弋矶山医院心血管内科, 芜湖241001, 安徽
  • 收稿日期:2008-07-02 修回日期:2008-08-03 出版日期:2008-09-26 发布日期:2020-10-13
  • 作者简介:杨玉雯, 女, 学士, 副教授, 主任医师, 主要研究方向:高血压基础与临床。Tel:0553-5682253 E-mail:kong.dylan@yahoo.com.cn

Effects of valsartan on nuclear factor-κB protein expression in the kidney of spontaneously hypertensive rats

YANG Yu-wen, WANG De-guo, KONG Xiang-quan, XU Chen-hua   

  1. Department of Cardiology, Yijishan Hospital, Wannan Medical College, Wuhu 241001, Anhui, China
  • Received:2008-07-02 Revised:2008-08-03 Online:2008-09-26 Published:2020-10-13

摘要: 目的:探讨自发性高血压大鼠(SHR) 肾组织NF-κB 原位表达变化以及AT1 受体阻断剂缬沙坦对其的影响。方法:16 只SHR 随机分成SHR组和SHR 加缬沙坦药物干预组(1 mg°kg-1°d-1),另8 只WKY 大鼠为正常对照组。分别在实验第2、4、6、8 周末测定大鼠尾动脉收缩压(SBP);实验结束取各组大鼠血浆测定血浆中肾素、血管紧张素II(AngII) 水平;取出各组大鼠两侧肾脏组织, 分别运用免疫组化原位测定肾组织中NF-κB 蛋白表达, 并进行半定量分析。结果:SHR 组SBP 和血浆中肾素活性以及AngII 水平与WKY 大鼠相比显著增高, 缬沙坦治疗组SBP 显著降低, 但血浆中肾素活性以及AngII 水平明显高于SHR 组和WKY 组。在蛋白水平,WKY 组大鼠肾组织中NF-κB 表达较低, SHR 组肾小球和肾小管中NF-κB 高度表达;使用缬沙坦干预后, NF-κB 表达显著降低。结论:在蛋白水平对NF-κB 表达的调控可能参与缬沙坦的降血压效应和肾保护作用。

关键词: 自发性高血压大鼠, 核因子-κB, 缬沙坦

Abstract: AIM: To observe the local expression of nuclear factor-κB (NF-κB) in spontaneously hypertensive rat (SHR) kidney and effects of AT1 receptor contagonist valsartan.METHODS: 16 SHRs were randomly divided into two groups:SHR control group and valsartan group.Another 8WKY rats act as normal control group.Systolic blood pressure (SBP) of SHR was measured at the beginning and the end of 2, 4, 6 and 8 weeks of intervention treatment.Radioimmunoassay was used to determine the activities of rennin and angiotensin II (AngII).The renal tissue NF-κB protein expression was detected by immunobiochemistry.RESULTS: SBP of SHR was remarkably decreased after valsartan intervention.However, the rennin activities and AngII level in plasma increased in valsartan group. In the renal tissue of SHR, there was remarkably increased in expression of NF-κB protein.Valsartan could significantly reduced NF-κB expression.CONCLUSION: Valsartan can depress NF-κB renal expression in protein level and might benefit hypotension renal function.

Key words: spontaneouslyhypertensiverat, nuclearfactor-κB, valsartan

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