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[热休克蛋白27对异氟醚预处理兔心肌缺血/再灌注损伤心肌的保护作用]

[Protective effect of heat-shock protein 27 on myocardium with isoflurane preconditioning in myocardial ischemia/reperfusion injury of myocardium in rabbit].

作者信息

Ran Ke, Zhu Rong, Lu Xiang-hang, Zou Ding-quan, Li Hui, Chang Ye-tian

机构信息

Department of Anesthesiology, Second Xiangya Hospital of South University, Changsha 410011, Hunan, China.

出版信息

Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2007 Nov;19(11):683-6.

Abstract

OBJECTIVE

To investigate the mechanism and the protective effect of heart-shock protein 27 (HSP27) on rabbit myocardium with isoflurane preconditioning in myocardial ischemia/reperfusion (I/R) injury.

METHODS

Thirty New Zealand white rabbits were randomly assigned to three groups (each n = 10):(1)Sham operation group (C group); (2)I/R group; (3)Two percent in volume is of isoflurane group (S group). S group was exposed to 2.0% isoflurane-pure oxygen for 2 hours. C group and I/R group were exposed 2 hours to pure oxygen to serve as untreated controls. Twenty-four hours later the rats in I/R group and S group underwent 40 minutes of coronary occlusion followed by 120 minutes of reperfusion. At the end of the reperfusion, infarct size (IS) was defined by Evan's blue and triphenyltetrazolium chloride (TTC) staining. Blood samples were taken from arterial line for determination of malondialdehyde (MDA) levels. Western Blotting was used to determine the expression of HSP27 and nuclear factor-KappaB (NF-KappaB) in myocardium.

RESULTS

Isoflurane preconditioning could decrease I/R induced myocardial infarct size [(19.7 +/- 2.8)% vs.(37.8 +/- 1.7)%]. This was accompanied by an increase in the expression in HSP27 [(84.5 +/- 4.3) gray scale value vs. (53.1 +/- 3.8) gray scale value] and a decrease in NF-KappaB [(58.6 +/- 4.2) gray scale value vs. (119.3+/-5.6) gray scale value] and MDA [(5.24 +/- 0.45)kU/L vs. (9.42 +/- 0.83)kU/L].

CONCLUSION

The expression of HSP27 induced by isoflurane preconditioning plays an important role in protecting myocardium against ischemia/reperfusion injury.

摘要

目的

探讨热休克蛋白27(HSP27)对异氟烷预处理兔心肌缺血/再灌注(I/R)损伤的作用机制及保护作用。

方法

30只新西兰白兔随机分为三组(每组n = 10):(1)假手术组(C组);(2)I/R组;(3)2%体积分数异氟烷组(S组)。S组暴露于2.0%异氟烷-纯氧环境2小时。C组和I/R组暴露于纯氧环境2小时作为未处理对照。24小时后,I/R组和S组大鼠进行40分钟冠状动脉闭塞,随后再灌注120分钟。再灌注结束时,用伊文思蓝和氯化三苯基四氮唑(TTC)染色法测定梗死面积(IS)。从动脉血管取血样测定丙二醛(MDA)水平。采用蛋白质免疫印迹法测定心肌中HSP27和核因子-κB(NF-κB)的表达。

结果

异氟烷预处理可减小I/R诱导的心肌梗死面积[(19.7±2.8)%对(37.8±1.7)%]。同时伴有HSP27表达增加[灰度值(84.5±4.3)对(53.1±3.8)]、NF-κB表达降低[灰度值(58.6±4.2)对(119.3±5.6)]和MDA水平降低[(5.24±0.45)kU/L对(9.42±0.83)kU/L]。

结论

异氟烷预处理诱导的HSP27表达在保护心肌免受缺血/再灌注损伤中起重要作用。

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