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缺血预适应通过抑制Smad 3蛋白表达减少心肌细胞凋亡的实验研究
引用本文:肖健,王志农,朱镇,黄盛东,徐志云,张宝仁.缺血预适应通过抑制Smad 3蛋白表达减少心肌细胞凋亡的实验研究[J].中国体外循环杂志,2008,6(4):241-243.
作者姓名:肖健  王志农  朱镇  黄盛东  徐志云  张宝仁
作者单位:第二军医大学附属长海医院胸心外科,上海,200433
摘    要:目的探讨Smad3蛋白(smallmother against decapentaplegic)在心肌细胞缺血再灌注损伤中与心肌细胞凋亡之间的关系。方法新生SD大鼠心肌细胞随机分为3组:①正常对照组(A组):在不含处理因素的含10%胎牛血清DMEM培养基在有氧培养箱(37℃、5%CO2和95%空气)中培养48h;②缺血再灌注(IR)诱导凋亡模型组(B组):不含血清的低糖DMEM培养基在缺氧培养箱(95%N2和5%CO2)中培养48h后,再用10%胎牛血清DMEM培养基在有氧培养箱中培养3h;③缺血预适应(IPC)组(C组):不含血清的低糖DMEM培养基在缺氧培养箱中培养6h后,再用10%胎牛血清DMEM培养基在有氧培养箱中培养3h,再进行缺血再灌注(步骤同B组)。结果A组、B组和C组心肌细胞凋亡率分别为(5.89±1.28)%、(26.68±6.17)%、(12.45±1.52)%,具有显著统计学差异。三组细胞Smad 3表达量分别为(21.77±2.32)%、(35.7±2.43)%、(29.47±1.36)%,具有显著统计学差异。结论Smad 3可以诱导心肌细胞缺血再灌注损伤后心肌细胞凋亡,而缺血预适应可抑制Smad 3的表达,从而保护心肌细胞。

关 键 词:缺血再灌注  缺血预适应  Smad  3  心肌细胞  凋亡

Study of Ischemic Preconditioning Reduce Apoptosis by Inhibited Smad 3
XIAO Jian,WANG Zhi-nong,ZHU Zhen,HUANG Sheng-dong,XU Zhi-yun,ZHANG Bao-ren.Study of Ischemic Preconditioning Reduce Apoptosis by Inhibited Smad 3[J].Chinese Journal of Extracorporeal Circulation,2008,6(4):241-243.
Authors:XIAO Jian  WANG Zhi-nong  ZHU Zhen  HUANG Sheng-dong  XU Zhi-yun  ZHANG Bao-ren
Institution:XIAO Jian,WANG Zhi-nong,ZHU Zhen,HUANG Sheng-dong,XU Zhi-yun,ZHANG Bao-ren.(Department of cardiothoracic surgery,Chang hai hospital,The Second Military Medical University,Shanghai 200433,China)
Abstract:OBJECTIVE To research the relationship of Smad 3 and myocardiocyte apoptosis stimulated by ischemia reperfusion injury(IR).METHODS The myocardiocytes of neonatal SD rats were divided randomly into 3 group.In group A(control group),the cells were cultured with modified DMEM with 10% FBS in a modified chamber and mixture gas(95%air and 5%CO2) for 48 hr;In group B(ischemia-reperfusion injury group),the cells were cultured with low carbohydrates DMEM under the condition of hypoxia(95% N2 and 5% CO2;the O2 parti...
Keywords:Smad 3
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