曾珑,余声欢,肖海茵,肖菲菲,朱蕊,邓春玉,杨慧,邝素娟,饶芳,魏薇

• 1:华南理工大学医学院
• 2:广东省医学科学院广东省人民医院

摘要(Abstract)：

目的 探讨转录辅激活因子p300是否参与调控心房肌细胞Kv1.5蛋白的表达。方法 以Western Blot检测细胞和C57BL/6小鼠心房组织p300蛋白、钾离子通道蛋白Kv1.5的表达。HL-1细胞在血管紧张素Ⅱ（AngⅡ）刺激的基础上使用p300抑制剂姜黄素或p300 siRNA干预，观察p300对Kv1.5蛋白表达以及超速延迟整流钾电流（I_(kur)）的作用。全细胞膜片钳技术检测各组细胞的I_(kur)和动作电位时程（APD）。快速起搏心房观察小鼠心房颤动（房颤）的可诱发性。结果 动物实验显示，与对照组相比，AngⅡ处理组小鼠有着明显更高的房颤诱发率（P<0.01），心耳组织p300以及Kv1.5蛋白表达明显升高（均P<0.05），而姜黄素干预后可以明显减少小鼠的房颤诱发率（P<0.01），并使p300和Kv1.5蛋白表达减少（P<0.05）。细胞实验显示，和对照组相比，AngⅡ处理组HL-1细胞p300以及Kv1.5蛋白表达明显升高（P<0.05),I_(kur)电流密度上升，APD缩短。在分别用p300抑制剂姜黄素和p300 siRNA干预后表现为p300和Kv1.5蛋白表达减少（P<0.05),I_(kur)电流密度下降，APD延长。结论 AngⅡ可通过p300引起心房肌细胞Kv1.5蛋白表达上升，I_(kur)电流密度上升，引起心房肌细胞电重构。

关键词(KeyWords)： p300;血管紧张素Ⅱ;心房颤动;Kv1.5蛋白;心房肌细胞

Abstract:

Keywords:

基金项目(Foundation): 国家自然科学基金青年科学基金项目（81900301）;; 广州市科技计划项目（201904010451）;广州市科技计划项目（201804010059）

作者(Author): 曾珑,余声欢,肖海茵,肖菲菲,朱蕊,邓春玉,杨慧,邝素娟,饶芳,魏薇

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