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氯沙坦对自发性高血压大鼠血管组织激肽释放酶表达的影响
引用本文:杨小虎,吕莎,彭应枝,余杨,岳影星,张勇.氯沙坦对自发性高血压大鼠血管组织激肽释放酶表达的影响[J].中国现代应用药学,2020,37(18):2206-2210.
作者姓名:杨小虎  吕莎  彭应枝  余杨  岳影星  张勇
作者单位:浙江医院,浙江医院,浙江医院,浙江医院,浙江医院,湖北医药学院
基金项目:浙江医院院级课题项目(编号:2015YJ038)、浙江中医药科学基金研究项目(编号:2017ZB002)
摘    要:目的:探讨氯沙坦(LST)对自发性高血压大鼠(SHR)血管组织Kallikrein表达的影响。方法:16只雄性自发性高血压大鼠随机分为模型组(Model)、氯沙坦组(LST)以及8只雄性Wistar-Kyoto大鼠(WKY)为空白组(Blank)。无创血压测量仪测量各组收缩压变化;Elisa试剂盒检测血清中激肽释放酶(Kallikrein)、一氧化氮(NO)及前列环素(PGI2)含量变化;苏木精-伊红(H&E)染色观察药物对主动脉病理学改变;实时定量qRT-PCR检测主动脉组织间Kallikrein基因表达变化;Western Blot检测主动脉组织中Kallikreinb蛋白表达变化。结果:SHR连续给药4周后,LST组收缩压呈时间依赖性下降;大鼠血清中Kallikrein、NO及PGI2分别上升了54.1%、49.5%及49.2%;组织病理学显示,LST组血管重构现象明显低于模型组;qRT-PCR显示,LST组的Kallicrein表达量上调了66.7%;Western Blot显示LST组Kallikrein蛋白表达与基因表达一致,呈正相关。结论:LST降低SHR血压及改善血管重构的作用可能与上调Kallikrein表达相关。

关 键 词:氯沙坦  高血压  血管重构  激肽释放酶
收稿时间:2019/1/22 0:00:00
修稿时间:2019/7/12 0:00:00

Effect of Losartan on Kallikrein Expression in Spontaneously Hypertensive Rat Aorta
YANG Xiaohu,LYU Sh,PENG Yingzhi,YU Yang,YUE Yingxing,ZHANG Yong.Effect of Losartan on Kallikrein Expression in Spontaneously Hypertensive Rat Aorta[J].The Chinese Journal of Modern Applied Pharmacy,2020,37(18):2206-2210.
Authors:YANG Xiaohu  LYU Sh  PENG Yingzhi  YU Yang  YUE Yingxing  ZHANG Yong
Institution:Zhejiang Hospital,Zhejiang Hospital,Zhejiang Hospital,Zhejiang Hospital,Zhejiang Hospital,Hubei Medical University
Abstract:OBJECTIVE: To investigate the effect of losartan on Kallikrein expression in spontaneously hypertensive rat aorta. METHODS: Sixteen female spontaneously hypertensive rats (SHR) were randomly divided into Model group, Losartan (LST) group while eight female normotensive Wistar-Kyoto rats (WKY) was Blank group. Non-invasive blood pressure (BP) measuring instrument monitored BP of each group rats in every week. The serum levels of total Kallikrein, NO and PGI2 were measured. Aorta change was evaluated with histopathologic examination by hematoxylin eosin (H&E) staining. Real time RT-PCR tested the gene expression change of Kallikrein. And the expression of Kallikrein in aortic tissue was measured by Western Blot. RESULTS: LST significantly decreased systolic BP in SHR group. Serum levels of Kallikrein, NO and PGI2 in LST group significantly increased more than those in the model group. Histopathologic examination indicated that vascular remodeling in LST group was reversed compared with model group. LST significantly reversed not only the up-regulation expression of Kallikrein gene but also Kallikrein protein in SHR group. CONCLUSION: LST decreasing systolic BP and improving vascular remodeling from SHR rats may be related to up-regulation of Kallikrein over-expression.
Keywords:Losartan  hypertension  vascular remodeling  Kallikrein
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