Protective Effect of Isoflurane on Myocardial Ischemia-Reperfusion Injury in Rats Through P38MAPK Signaling Pathway

被引:0
|
作者
Liu, Zheng [1 ]
Zhang, Mingming [1 ]
Wang, Mangyuan [1 ]
Zhu, Tao [1 ]
Huo, Qiang [1 ]
机构
[1] Xinjiang Med Univ, Affiliated Hosp 1, Dept Cardiac Surg, Urumqi 830054, Xinjiang, Peoples R China
关键词
I-R Injury; Isoflurane; P38MAPK; Apoptosis; Myocardium; INHIBITION; ACTIVATION; AUTOPHAGY;
D O I
10.1166/jbt.2020.2393
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Objective: Abnormal p38 MAPK activation involves in ischemia-reperfusion (IR) injury. Isoflurane (ISO) is a clinically used inhaled anesthetic and protects myocardial I-R injury. Our study assessed whether ISO exerts a protective role in myocardial I-R injury. Methods: Rat myocardial I-R injury model was set followed by analysis of p-p38 MAPK expression in myocardial tissue by western blot, caspase-3 activity, as well as MDA and SOD content. Rats were assigned into Sham group, IR group, I-R + ISO group, followed by measuring p-p38 MAPK expression, caspase-3 activity, MDA and SOD, cell apoptosis and ROS content. Results: Compared with Sham group, MDA content, caspase-3 activity and p-p38 MAPK protein expression as well as ROS content and apoptosis rate in I-R model rats were significantly increased and SOD activity was significantly decreased. ISO pretreatment significantly reduced MDA content, caspase-3 activity, ROS content and apoptosis rate in I-R model rats, increased SOD activity and reduced p-p38 MAPK expression. Conclusion: Activation of p38MAPK signaling plays a role in mediating myocardial IR injury and cardiomyocyte apoptosis. ISO pretreatment inhibits oxidative stress and cardiomyocyte apoptosis and protects myocardial IR injury via inhibiting p38MAPK signaling.
引用
收藏
页码:1225 / 1230
页数:6
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