α1a和at1受体通过特定pkc亚型调节herg钾通道的分子基础

α1a和at1受体通过特定pkc亚型调节herg钾通道的分子基础

ID:34864847

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时间:2019-03-12

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1、授予单位代码10089学号或申请号20122646HebeiMedicalUniversity硕士学位论文科学学位alA和ATI受体通过特定PKC亚型调节hERG钾通道的分子基础研究生:申丽导师:许彦芳教授专业:药理学二级学院:基础医学院2015年3月河北医科大学学位论文使用授权及知识产权归属承诺本学位论文在导师(或指导小组)的指导下,由本人独立完成。本丨学位论文研究所获的研究成果,其知识产权归河北医科大学所有。河北医科大学有权对本学位论文进行交流、公幵和使用。凡发表与学位论文主要内容相关的论文,第一署名单位为河北医科大学,试验材料、原始数据、申报的专利等知识产权均归河北医科大学所有。否则,承

2、担相应的法律责任。A月…曰河北医科大学研究生学位论文独创性声明本论文是在导师指导下进行的研究工作及取得的研究成果,除了文中特别加以标注和致谢等内容外,文中不包含其他人己经发表或撰写的研究成果,指导教师对此进行了审定。本论文由本人独立撰写,文责自负。目录中文摘要·············································································1英文摘要·············································································5英文缩写······

3、·······································································9研究论文1A和AT1受体通过特定PKC亚型调节hERG钾通道的分子基础前言···········································································10材料与方法··································································11结果······································

4、·····································21附图···········································································22附表···········································································30讨论···········································································32结论······················

5、·····················································33参考文献·····································································34综述内吞作用对心脏电压依赖钾通道的调节···························38致谢·················································································48个人简历·································

6、··········································491中 文 摘 要 1A和AT1受体通过特定PKC亚型调节hERG钾通道的分子基础摘要心律失常,尤其是严重的室性心律失常,是致心血管病患者死亡的主要原因之一。揭示心律失常发生的细胞分子机制,对于心血管疾病治疗有重要意义。先天遗传基因改变或后天获得性因素引起心肌离子通道的结构[1-5]和/或功能紊乱是产生心律失常的重要分子基础。其中获得性离子通道功能的改变与神经体液系统的过度激活(特别是交感肾上腺素和肾素-血管紧张素-醛固酮系统)密切相关。已有大量文献报道,肾上腺素1A受体和血管紧张素II(AngII)AT

7、1受体可调节心肌细胞膜上的离子通道功[6-10]能,是心血管疾病病理情况下通道功能异常的重要原因。蛋白激酶C(proteinkinaseC,PKC)作为细胞功能调控的重要分子,[11-19]中介多种神经体液因子作用,在离子通道功能调节中发挥重要作用。依据PKC结构与激活机制分为三类:传统型PKC(cPKC,包括α、βI、βII和γ),新型PKC(nPKC,包括δ、ε、π和θ),非典型PKC(aPK

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