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脊髓丝裂原活化蛋白激酶-细胞外信号调节激酶信号通路在心肌缺血再灌注损伤中的作用

[Role of spinal MAPK-ERK signal pathway in myocardial ischemia-reperfusion injury].

作者信息

Jiang Meng, Wang Lin, Jiang Hai-He

机构信息

Department of Cardioathoracic Surgery, Xiangya Hospital of Central South University, Changsha 410008, China.

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2013 May;15(5):387-91.

PMID:23676945
Abstract

OBJECTIVE

To explore the role of spinal MAPK-ERK signal pathway in myocardial ischemia-reperfusion (I/R) injury.

METHODS

Sixty male Sprague-Dawley(SD) rats (80-100 g) were randomly divided into 3 groups: sham (n=10), PD98059 (n=25) and I/R groups (n=25). Three days after successful intrathecal implantation, 5 μg DMSO was injected intrathecally into the sham group, and then the left coronary arteries were separated without being tied. Rats in the I/R and PD98059 groups were injected with 5 μL DMSO and PD98059 (5 μg) 30 minutes before thoractomy respectively. Then the left coronary artery was tied for 30 minutes followed by 120 minutes of reperfusion. After the experiments, the ERK phosphorylation condition of T1-T4 spinal cord segments was detected with immunofluorescence; the myocardiac apoptosic index and infarct size were measured.

RESULTS

Expression of p-ERK in the I/R group was significantly higher than in the sham and PD98059 groups (P<0.05). Myocardial apoptotic index and infarct size in the PD98059 group were significantly lower than in the I/R group (P<0.05), but higher in the PD98059 group than in the sham group (P<0.05).

CONCLUSIONS

The MAPK-ERK pathway in the superior thorathic spinal cord can be activated by myocardial ischemia-reperfusion and inhibition of the pathway can play a protective role in myocardial ischemia-reperfusion injury.

摘要

目的

探讨脊髓丝裂原活化蛋白激酶-细胞外信号调节激酶(MAPK-ERK)信号通路在心肌缺血再灌注(I/R)损伤中的作用。

方法

将60只雄性Sprague-Dawley(SD)大鼠(80-100 g)随机分为3组:假手术组(n=10)、PD98059组(n=25)和I/R组(n=25)。鞘内植入成功3天后,向假手术组鞘内注射5μg二甲基亚砜(DMSO),然后分离左冠状动脉但不结扎。I/R组和PD98059组大鼠在开胸术前30分钟分别注射5μL DMSO和5μg PD98059。然后结扎左冠状动脉30分钟,再灌注120分钟。实验结束后,用免疫荧光法检测T1-T4脊髓节段的ERK磷酸化情况;测量心肌凋亡指数和梗死面积。

结果

I/R组p-ERK的表达明显高于假手术组和PD98059组(P<0.05)。PD98059组心肌凋亡指数和梗死面积明显低于I/R组(P<0.05),但高于假手术组(P<0.05)。

结论

胸段脊髓的MAPK-ERK通路可被心肌缺血再灌注激活,抑制该通路可对心肌缺血再灌注损伤起到保护作用。

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