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异丙酚对大鼠心肌缺血/再灌注损伤m-钙激活蛋白酶及线粒体膜通透性的影响

Effects of Propofol on the Activation of m-Calpian and the Mitochondrial Permeability Transition of the Rat Ischemia-Reperfusion Myocardium

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【作者】 朱俊超马虹王俊科

【Author】 ZHU Jun-chao,MA Hong,WANG Jun-ke (Department of Anesthesiology,The First Affiliated Hospital,China Medical University,Shenyang 110001,China)

【机构】 中国医科大学附属第一医院麻醉科中国医科大学附属第一医院麻醉科 沈阳110001沈阳110001

【摘要】 目的观察异丙酚对大鼠在体缺血/再灌注损伤心肌m-钙激活蛋白酶(m-calpain)激活和线粒体膜通透性转运的影响,探讨异丙酚对心肌缺血/再灌注损伤的保护机制。方法选用健康SD雄性大鼠24只,随机分为3组(n=8),假手术组(Sham组)、缺血/再灌注组(I/R组)、异丙酚组(P组)。分别在结扎左冠状动脉(LV)前即刻(T1)、缺血30min即刻(T2)及LV松开再灌注120min即刻(T3)3个时间点抽取动脉血2ml检测血浆超氧化物岐化酶(SOD)活性、丙二醛(MDA)和肌钙蛋白I(cTnI)浓度,免疫组织化学SP法检测各组大鼠m-calpain水平。结果与T1时间点相比,T2、T3时间点的血浆SOD活性降低(P<0.05),MDA及cTnI浓度升高(P<0.05);与T2时间点相比,T3时间点的血浆SOD活性降低(P<0.05),MDA及cTnI浓度升高(P<0.05)。在T2时间点,与I/R组相比,P组的血浆SOD活性升高(P<0.05),MDA及cTnI浓度降低(P<0.05);在T3时间点,与I/R组相比,P组的血浆SOD活性升高(P<0.05),MDA及cTnI浓度降低(P<0.05)。与对照组相比,I/R组和P组m-calpain水平均升高,与I/R组相比,P组m-calpain水平降低(P<0.05)。结论异丙酚对缺血/再灌注损伤心肌具有保护作用,通过抑制心肌缺血/再灌注损伤过程中m-calpain的激活而减轻缺血/再灌注损伤时线粒体膜通透性转运是其保护机制之一。

【Abstract】 Objective To observe the effects of propofol on the activation of m-calpain and the mitochondrial permeability transition of ischemia-reperfusion myocardial myocytes. Methods 24 healthy male SD rats weighing 250~350 mg were divided into 3 groups (n =8 each):(1)control group,(2)ischemia/reperfusion(I/R) group,(3)propofol group. Blood sample was taken from femoral artery at three time points to assay the concentration of MDA,SOD and cTnI. Results Compared with T1,the SOD activity at T2~T3 was lower(P < 0.05),and the MDA concentration and cTnI level were higher(P < 0.05)in both groups. Compared with T2,the SOD activity was lower(P < 0.05)at T3,and the concentration of MDA and cTnI level were higher(P < 0.05)in both groups. Compared with I/R Group,at the T2 and T3 points,the SOD activity was higher in P Group(P < 0.05),and MDA concentration and cTnI level were lower in P Group(P < 0.05); the SOD activity in P Group at T3 was higher than that of I/R group(P < 0.05),and the concentration of MDA and cTnI level were lower(P < 0.05). Conclusion To inhibit the activation of m-calpain in ischemia-reperfusion injury cadiocytes and decrease the MPT is one of the protective mechanisms of propofol on myocardium which have undergone ischemia-reperfusion injury.

【基金】 国家自然科学基金资助项目(30371376)
  • 【文献出处】 中国医科大学学报 ,Journal of China Medical University , 编辑部邮箱 ,2008年03期
  • 【分类号】R96
  • 【被引频次】1
  • 【下载频次】139
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