军事医学
軍事醫學
군사의학
Military Medical Sciences
2015年
9期
682-687
,共6页
孟宪卿%杨传华%吴赛%姜月华%吴波
孟憲卿%楊傳華%吳賽%薑月華%吳波
맹헌경%양전화%오새%강월화%오파
肥胖症%高血压%大鼠%受体,瘦素%水通道蛋白质2
肥胖癥%高血壓%大鼠%受體,瘦素%水通道蛋白質2
비반증%고혈압%대서%수체,수소%수통도단백질2
obesity%hypertension%rat%receptors,leptin%aquaporin 2
目的:观察肥胖性高血压大鼠(OHR)肾脏瘦素(Lep)受体(LepR)与水通道蛋白2(AQP2)表达的情况,探讨OHR Lep抵抗机制及肾在高Lep血症作用下的病理改变。方法由高脂饮食诱导建立OHR模型,与自发性高血压大鼠( SHR)和正常Wistar大鼠对照。应用酶联免疫吸附法( ELISA)检测大鼠血清中甘油三酯( TG)、总胆固醇(TC)、Lep、血管加压素(AVP)、血管紧张素Ⅱ(AngⅡ)、β2微球蛋白(β2-MG)变化,光镜下观察肾组织的形态结构,实时荧光定量PCR检测肾LepR与AQP2的mRNA表达,蛋白免疫印迹法检测相关蛋白表达情况。结果与正常对照组比较,模型组大鼠血中TG、TC、Lep、AVP、AngⅡ、β2-MG均明显升高(P<0.05),大鼠肾LepR、AQP2的mRNA表达上调(P<0.05)。与SHR组比较,大鼠血清中TG、TC、Lep升高。模型组大鼠血清中Lep与血清中β2-MG、AVP呈线性相关(R2=0.87;R2=0.95)。结论肾参与OHR水代谢紊乱和Lep抵抗的病理过程,可能是肥胖导致高血压的重要机制之一。
目的:觀察肥胖性高血壓大鼠(OHR)腎髒瘦素(Lep)受體(LepR)與水通道蛋白2(AQP2)錶達的情況,探討OHR Lep牴抗機製及腎在高Lep血癥作用下的病理改變。方法由高脂飲食誘導建立OHR模型,與自髮性高血壓大鼠( SHR)和正常Wistar大鼠對照。應用酶聯免疫吸附法( ELISA)檢測大鼠血清中甘油三酯( TG)、總膽固醇(TC)、Lep、血管加壓素(AVP)、血管緊張素Ⅱ(AngⅡ)、β2微毬蛋白(β2-MG)變化,光鏡下觀察腎組織的形態結構,實時熒光定量PCR檢測腎LepR與AQP2的mRNA錶達,蛋白免疫印跡法檢測相關蛋白錶達情況。結果與正常對照組比較,模型組大鼠血中TG、TC、Lep、AVP、AngⅡ、β2-MG均明顯升高(P<0.05),大鼠腎LepR、AQP2的mRNA錶達上調(P<0.05)。與SHR組比較,大鼠血清中TG、TC、Lep升高。模型組大鼠血清中Lep與血清中β2-MG、AVP呈線性相關(R2=0.87;R2=0.95)。結論腎參與OHR水代謝紊亂和Lep牴抗的病理過程,可能是肥胖導緻高血壓的重要機製之一。
목적:관찰비반성고혈압대서(OHR)신장수소(Lep)수체(LepR)여수통도단백2(AQP2)표체적정황,탐토OHR Lep저항궤제급신재고Lep혈증작용하적병리개변。방법유고지음식유도건립OHR모형,여자발성고혈압대서( SHR)화정상Wistar대서대조。응용매련면역흡부법( ELISA)검측대서혈청중감유삼지( TG)、총담고순(TC)、Lep、혈관가압소(AVP)、혈관긴장소Ⅱ(AngⅡ)、β2미구단백(β2-MG)변화,광경하관찰신조직적형태결구,실시형광정량PCR검측신LepR여AQP2적mRNA표체,단백면역인적법검측상관단백표체정황。결과여정상대조조비교,모형조대서혈중TG、TC、Lep、AVP、AngⅡ、β2-MG균명현승고(P<0.05),대서신LepR、AQP2적mRNA표체상조(P<0.05)。여SHR조비교,대서혈청중TG、TC、Lep승고。모형조대서혈청중Lep여혈청중β2-MG、AVP정선성상관(R2=0.87;R2=0.95)。결론신삼여OHR수대사문란화Lep저항적병리과정,가능시비반도치고혈압적중요궤제지일。
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.