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芬太尼和脂多糖迟发预处理对缺血再灌注损伤大鼠心肌细胞凋亡的影响
引用本文:朱志军,高云霞,刘伟华. 芬太尼和脂多糖迟发预处理对缺血再灌注损伤大鼠心肌细胞凋亡的影响[J]. 中国现代医药杂志, 2008, 10(11)
作者姓名:朱志军  高云霞  刘伟华
作者单位:辽宁电力中心医院麻醉科,辽宁沈阳,110015
摘    要:
目的 诱导大鼠心肌迟发预处理保护作用,测定心肌细胞凋亡率、Caspase、细胞色素C的变化.探讨DPC对心肌细胞凋亡的影响及作用机制.方法 健康SD大鼠32只,随机分为4组,每组8只.芬太尼组(A组):大鼠腹腔注射芬太尼,24小时后建垃缺血再灌注损伤模型;脂多糖组(B组):腹腔注射脂多糖,24小时后处理同A组.生理盐水组(C组):腹腔注射生理盐水,24小时后处理同A组.对照组(D组):不注射任何药物,24小时后处理同A组.TUNEL法检测心肌细胞凋亡;caspase-3试剂盒测定其活性;Western blot法检测细胞色素C.结果 HE染色:损伤重区域的心肌仍保存细胞轮廓,横纹不清或消失,收缩带形成.损伤轻区域细胞轮廓清晰.横纹不消失.TUNEL染色:散在的细胞核呈棕色凋亡细胞.A组和B组心肌细胞凋亡毕分别为(9±3)%和(11±3)%低于C组(17±5)%;A组和B组caspase-3活性(分别为0.43±0.11和0.40±0.13)低于C组(0.75±0.23);A组和B组细胞色素C蛋白表达(分别为0.67±0.11和0.63±0.18)低于C组(0.98±0.19),均有显著差异(P<0.05).结论 芬太尼、脂多糖诱导的迟发预处理中存在心肌细胞凋亡.且心肌细胞凋亡率、细胞色素C、Caspase-3降低.

关 键 词:芬太尼  脂多糖  迟发预处理  缺血再灌注损伤  凋亡

Role of delayed preconditioning on apoptosis of rat myocardium induced by fentanyl and lipopolysaccharide
Zhu Zhi-jiu,Gao Yunxia,Liu Weihua. Role of delayed preconditioning on apoptosis of rat myocardium induced by fentanyl and lipopolysaccharide[J]. Modern Medicine Journal of China, 2008, 10(11)
Authors:Zhu Zhi-jiu  Gao Yunxia  Liu Weihua
Affiliation:Zhu Zhi-jun,Gao Yunxia,Liu Weihua.Department of Anesthesiology,Liaoning Power Center Hospital,Shenyang 110015
Abstract:
Objective To measure the apoptosis rate,Actavity of caspase-3,and Cytochrome C in the process of delayed preconditioning on rat myocardium,try to reveal their association and to manifest the role of delayed preconditioning on apoptosis of rat myocardium.Methods Thirty two SD rats were randomized into four groups(n=8),fentanyl group(group A) were admin-istrated with fentanyl by peritoneal injection,then the heart underwent ischemic reperfusion injury in vivo after 24 hours.LPS group(group B)and NS group(grou...
Keywords:Fentanyl Lipopolysaccharide Delayed preconditioning Ischemic reperfusion injury Apoptosis  
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