慢性应激对大鼠肾脏水通道蛋白1的影响及机制研究  

Effect of chronic stress on renal aquaporin-1 expression in rats and its mechanism

作　　者：朱叶 卫郅星 陈晓帆 张国兴[1] Ye Zhu;Zhi-xing Wei;Xiao-fan Chen;Guo-xing Zhang(Department of Physiology, School of Basic Medicine and Biological Sciences, Medical College of Soochow University, Suzhou, Jiangsu 215123, China)

机构地区：[1]苏州大学医学部基础医学与生物科学学院生理学系,江苏苏州215123

出　　处：《中国现代医学杂志》2017年第28期1-5,共5页China Journal of Modern Medicine

基　　金：国家自然科学基金(No:81270316;81470563);国家级大学生创新训练项目(No:2015suda047)

摘　　要：目的研究慢性应激(足底电击)对大鼠肾脏水通道蛋白1(AQP1)的影响及其机制。方法以足底电击SD雄性大鼠为慢性应激模型,分为对照组、电击组、肾交感神经切除组、肾交感神经切除+电击组、注射血管紧张素转换酶抑制剂(卡托普利)+电击组、注射抗氧化剂(Tempol)+电击组,每组6只大鼠。应用尾套法测量大鼠的血压,实时荧光定量聚合酶链反应(qRT-PCR)测定各组大鼠肾脏AQP1 mRNA的表达变化,免疫组织化学法(IHC)观察AQP1在各组大鼠肾脏中的表达及分布。结果电击组大鼠肾脏AQP1及血压与对照组比较,均差异有统计学意义(P<0.05),电击组大鼠肾脏AQP1表达明显,血压升高;肾交感神经切除组大鼠肾脏AQP1与对照组比较,差异有统计学意义(P<0.05),AQP1表达减少,血压未见升高。肾交感神经切除+电击组、注射卡托普利+电击组、注射Tempol+电击组大鼠肾脏AQP1表达及血压与电击组比较,差异有统计学意义(P<0.05),肾脏AQP1表达均减少,血压均降低。结论交感神经可调节AQP1的表达,足底电击通过兴奋肾交感神经上调AQP1,另外,AQP1还受氧化应激及肾素-血管紧张素系统调控。AQP1在慢性应激诱导的高血压中可能起着一定的作用。Objective To investigate the effect of chronic stress(induced by foot shock)on renal aquaporin-1(AQP1)expression in rats and its mechanism.Methods The chronic stress model was established in male Sprague-Dawley(SD)rats by foot shock.The rats were divided into control group,foot shock group,renal sympathetic nervedenervation group,renal sympathetic nerve denervation plus foot shock group,Captopril plus foot shock group andTempol plus foot shock group(6in each group).Tail-cuff method was applied to measure blood pressure of therats.RT-PCR was applied to detect the AQP1mRNA level in the kidney tissues.Immunohistochemistry was usedto observe the expression and distribution of AQP1in rat kidneys.Results Compared to the control group,theexpression of AQP1and the blood pressure markedly increased in the foot shock group(P<0.05),the expressionof AQP1in the kidney tissues was decreased in the renal sympathetic nerve denervation group(P<0.05)withoutsignificant increase of blood pressure.Compared to the foot shock group,the expression of AQP1was decreased inthe renal sympathetic nerve denervation plus foot shock group,the Captopril plus foot shock group and the Tempolplus foot shock group accompanied by reduction of blood pressure(P<0.05).Conclusions Renal AQP1expressionin rats is regulated by sympathetic nerves.Foot shock causes the increase of AQP1expression,which is due to the increased renal sympatheic activity.In addition,oxidative stress and renin-agiontensin system regulate the expressionof AQP1.AQP1may play a certain role in the regulation of hypertension induced by chronic stress.

关 键 词：水通道蛋白1 应激性高血压 氧化应激 肾交感神经 

分 类 号：R363[医药卫生—病理学]