文章摘要
张彦清,岳毅,陈斌.丙泊酚对缺血再灌注诱导心肌细胞凋亡的影响[J].山西医科大学学报,2007,38(11):965~967
丙泊酚对缺血再灌注诱导心肌细胞凋亡的影响
Effect of propofol on myocardial apoptosis induced by ischemia reperfusion
  
DOI:
中文关键词: 再灌注损伤  丙泊酚  凋亡
英文关键词: reperfusion injury  propofol  apoptosis
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张彦清,岳毅,陈斌 1山西医科大学第一临床医学院麻醉科太原0300012山西武警总院神经外科3大同市第二人民医院骨科 sxtyzyq@sina.com 
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中文摘要:
      目的 探讨丙泊酚对大鼠心肌缺血/再灌注(MI/R )后心肌细胞凋亡的影响及其作用机制。 方法 选用250-300 g雄性SD大鼠,制备大鼠MI/R模型[3],给 以45 min缺血和2 h、4 h再灌注。根据实验目的,将45只SD大鼠随机均分为3组(n=15) 。 假手术组(sham组):在冠状动脉前降支(LAD)下穿线,但不结扎,其余操作与其他各 组相同;单纯MI/R组(MI/R组):大鼠接受MI/R处理;丙泊酚组(P组):大鼠接受MI/R处 理,在再灌注期间给以0.42 mg/(kg·h)丙泊酚。再灌注结束后采用DNA原位末端缺口标记 技术(TUNEL)测定心肌细胞凋亡比例,免疫组化法测定心肌细胞内抗凋亡分子Akt、Bcl 2 和促凋亡分子p38 MAPK的表达。 结果 与假手术组比较,丙泊酚组MI/R诱导的心肌组织的凋亡明显降低(P<0.05)。免疫组化的结果显示,丙泊酚组肌内Akt和Bcl 2的形成增加, p38 MA PK的水平降低(P<0.05)。 结论 本实验结果提示丙泊酚对MI/R后的心肌组织有显著的保护作用, 它的这种作用与其对Akt、Bcl 2和p38 MAPK的影响密切相关。
英文摘要:
      Objective To explore the effect of propofol on myocradial apoptosi s induced by myocardial ischemia reperfusion(MI/R) and its potential mechanism . Methods Forty five Wistar rats weighing 250-300 g were rando m ly divided into three groups: sham operation group (0.9% NaCl);MI/R group; pr opofol group [intravenous infusion 0.42 mg/(kg·h) during reperfusion ]. At the end of reperfusion, the ratio of myocardial apoptosis was analyzed wi th TUNEL assay, and the expression of pAkt, p38 MAPK and Bcl 2 was detected with immunohistochemical staining. Results Compared with sham operation group, myocardial apopto sis decreased significantly in propofol group. The expression of pro apoptotic p38 MA PK decreased in propfol group, but the expression of anti-apoptotic proteins Akt and Bcl 2 significantly increased in cadiomyocytes. Conclusion These results indicate that propofol is more likel y to protect cardiomyocytes from the injury of MI/R induced apoptosis by incre asing production of anti apoptotic proteins. 
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