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丙泊酚对大鼠心肌缺血再灌注损伤的保护作用
引用本文:解丽君,张建新,李兰芳,张勤增,郝娜,李立萍,李国风. 丙泊酚对大鼠心肌缺血再灌注损伤的保护作用[J]. 中国药理学与毒理学杂志, 2011, 25(1): 7-12. DOI: 10.3867/j.issn.1000-3002.2011.01.002
作者姓名:解丽君  张建新  李兰芳  张勤增  郝娜  李立萍  李国风
作者单位:河北省医学科学院药物所药理学研究室,河北,石家庄,050021
摘    要:
目的 探讨异丙酚的心肌保护作用及机制.方法 阻断大鼠左冠状动脉前降支30 min,再灌注2 h引起心肌缺血再灌注(I/R)损伤.缺血前10 min分别灌注异丙酚3,6及12 mg·kg-1至再灌12 h后实验结束.记录心率和平均动脉压,并计算心率-血压指数;光镜电镜观察心肌组织的形态学变化;原位末端标记检测心肌细胞凋亡...

关 键 词:丙泊酚  心肌再灌注损伤  核因子-κB  胱天蛋白酶3
收稿时间:2010-03-09

Protective effect of propofol on myocardium ischemia/reperfusion injury in rats
XIE Li-jun,ZHANG Jian-xin,LI Lan-fang,ZHANG Qin-zeng,HAO Na,LI Li-ping,LI Guo-feng. Protective effect of propofol on myocardium ischemia/reperfusion injury in rats[J]. Chinese Journal of Pharmacology and Toxicology, 2011, 25(1): 7-12. DOI: 10.3867/j.issn.1000-3002.2011.01.002
Authors:XIE Li-jun  ZHANG Jian-xin  LI Lan-fang  ZHANG Qin-zeng  HAO Na  LI Li-ping  LI Guo-feng
Affiliation:XIE Li-jun,ZHANG Jian-xin,LI Lan-fang,ZHANG Qin-zeng,HAO Na,LI Li-ping,LI Guo-feng(Department of Pharmacology,Institute of Materia Medica,Hebei Academy of Medical Sciences,Shijiazhuang 050021,China)
Abstract:
OBJECTIVE To explore molecular mechanisms of propofol in myocardial protection. METHODS Rat myocardium ischemia/reperfusion(I/R) injury was induced by occluding the left main coronary artery for 30 min and reperfusing for 2 h. Propofol 3, 6 and 12 mg·kg-1 was intravenously given 10 min before ischaemia till the end of experiment. Heart rate (HR) and mean arterial blood pressure (MAP) were recorded, and pressure- rate index (PRI) was calculated. The pathological changes of myocardium were examined by light and electron microscopy. Translocation of NF- κB in the cardiomyocytes was detected by immunohistochemistry. Expressions of NF- κB and caspase 3 were determined by Western blotting. The incidence of cardiomyocyte apoptosis was detected by TdT-mediated dUTP nick end labeling staining. RESULTS The cardiac function parameters (MAP, PRI) in I/R group were lower than those of sham group (P<0.05). Compared with I/R group, propofol 6 and 12 mg·kg-1 resulted in improvement in MAP and PRI, respectively (P<0.05). The pathological changes of myocardium induced by I/R injury, such as cardiomyocyte swelling and mitochondrial membrane swelling, the cristae disruption were significantly alleviated by propofol 6 and 12 mg·kg-1. Compared with sham control group, expression of NF-κB in the nuclei markedly increased in I/R group (P<0.05). In addition, expression of capase 3 and apoptosic index were significantly increased (P<0.05). Compared with I/R group, propofol 6 and 12 mg·kg-1 significantly attenuated expression of NF-κB in the nuclei (P<0.05), decreased expression of caspase 3 in myocardium (P<0.05) and inhibited occurrence of cardiomyocytes apoptosis. CONCLUSION Propofol can inhibit NF-κB activation and down- regulate the expression of caspase 3 and as a result suppress cardiomyocytes apoptotic initation during the myocardium I/R injury, which may be one of the molecular mechanisms of its cardioprotection.
Keywords:propofol  myocardial reperfusion injury  nuclear factor-κB  caspase 3
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