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肥胖性高血压大鼠肾脏瘦素受体及水通道蛋白2的表达

孟宪卿 杨传华 吴赛 姜月华 吴波

军事医学Issue(9):682-687,6.
军事医学Issue(9):682-687,6.DOI:10.7644/j.issn.1674-9960.2015.09.008

肥胖性高血压大鼠肾脏瘦素受体及水通道蛋白2的表达

Expression of leptin receptor and aquaporin 2 in kidneys of obesity-related hyperten-sive rats

孟宪卿 1杨传华 2吴赛 3姜月华 1吴波3

作者信息

  • 1. 山东中医药大学,济南 250355
  • 2. 山东中医药大学附属医院,济南 250011
  • 3. 山东中医药大学附属医院,济南 250011
  • 折叠

摘要

Abstract

Objective To observe the expression of leptin(Lep) receptor (LepR) and aquaporin 2 (AQP2) in the kidneys of obesity-related hypertensive rats ( OHR ) and to explore the mechanism of Lep resistance and water metabolic disorders in them.Methods OHR( model group) were induced by high-fat diet.Normal Wistar rats were chosen as normal control and hypertensive rats(SHR) as positive control.The serum level of triglycerides(TG), total cholesterol(TC), Lep, vasopressin ( AVP ) , angiotensinⅡ( AngⅡ) and β2-microglobulin (β2-MG ) was measured by enzyme linked immunosorbent assays ( ELISA) and renal morphology was observed by HE staining.The density of LepR and AngⅡtype 1( AT1) in the kidney was observed by immunohistochemistry.mRNA And protein expression of LepR and AQP2 in the kidney was assayed by real-time polymerase chain reaction and Western blotting.Results Compared with normal rats,the TG, TC, Lep, AVP, AngⅡand β2-MG of the model group were significantly increased (P<0.05), and protein and mRNA expression of LepR and AQP2 in the kidney were up-regulated (P<0.05).Compared with SHR group, TG, TC and Lep in serum of the model group were significantly increased (P<0.05).The concentrations of AVP,β2-MG and Lep was linearly related(R2 =0.87,R2 =0.95).Conclusion Water metabolic disorder and Lep resistance may be involved in the kidney injury of OHR, which may be one of the important pathogeneses of obesity-related hypertension.

关键词

肥胖症/高血压/大鼠/受体,瘦素/水通道蛋白质2

Key words

obesity/hypertension/rat/receptors,leptin/aquaporin 2

分类

医药卫生

引用本文复制引用

孟宪卿,杨传华,吴赛,姜月华,吴波..肥胖性高血压大鼠肾脏瘦素受体及水通道蛋白2的表达[J].军事医学,2015,(9):682-687,6.

基金项目

泰山学者岗位建设资金资助项目(2012-55);山东省科技发展计划资助项目(2014GSF119011);山东省自然科学基金资助项目 ()

军事医学

OA北大核心CSCDCSTPCD

1674-9960

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