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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.
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页码:1225 / 1230
页数:6
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