Role of carvacrol in cardioprotection against myocardial ischemia/reperfusion injury in rats through activation of MAPK/ERK and Akt/eNOS signaling pathways

被引：84

作者：

Chen, Yunping ^{[1
]}

Ba, Lina ^{[1
]}

Huang, Wei ^{[1
]}

Liu, Yan ^{[1
]}

Pan, Hao ^{[1
]}

E, Mingyao ^{[1
]}

Shi, Pilong ^{[1
]}

Wang, Ye ^{[1
]}

Li, Shuzhi ^{[1
]}

Qi, Hanping ^{[1
]}

Sun, Hongli ^{[1
]}

Cao, Yonggang ^{[1
]}

机构：

[1] Harbin Med Univ Daqing, Dept Pharmacol, Daqing 163319, Peoples R China

来源：

EUROPEAN JOURNAL OF PHARMACOLOGY | 2017年 / 796卷

关键词：

Carvacrol; Myocardial ischemia/reperfusion injury; MAPK/ERK; Akt/eNOS; APOPTOTIC CELL-DEATH; ISCHEMIA-REPERFUSION; PROTEIN-KINASE; PROTECTION; INSULIN; AKT;

D O I：

10.1016/j.ejphar.2016.11.053

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Carvacrol (CAR) is a compound isolated from some essential oils, many studies have demonstrated its therapeutic potential on different diseases. This study aims to evaluate the protective effect of CAR against myocardial ischemia/reperfusion (I/R) injury in rats. Male adult rats underwent ligation of the left anterior descending coronary artery (LAD) in I/R models. Rats were treated with CAR after LAD. The levels of I/R-induced infarct size, cardiomyocyte apoptosis and cardiac functional impairment were examined. Levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) were detected by western blotting. Cardiornyocytes induced by hypoxic reperfusion (H/R) injury were tested by Hoechst 33258. Our results revealed that CAR administration significantly protected the heart function, attenuated myocardial infarct size, increased SOD and CAT levels, reduced MDA level and especially decreased cardiomyocytes apoptosis. Western blotting showed that CAR treatment up-regulated phosphorylated ERK (p-ERK), while producing no impact onp38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK). The cardioprotection of CAR was reversed by the ERK inhibitor PD-98059, demonstrating the involvement of the MAPK/ERK pathway in the anti-apoptotic mechanisms of CAR. Besides, the results in vitro also showed the protective efficiency of CAR on cardiomyocytes H/R injury. Furthermore, pretreatment with CAR markedly increased the activation of Akt/eNOS pathway in cardiomyocytes subjected to H/R, and the protective effects of CAR were abolished in the presence of the Aid inhibitor LY294002. Therefore, the cardioprotective effects of CAR may be attributed to its antioxidant and antiapoptotic activities through activations of the MAPK/ERK and Akt/eNOS signaling pathways.

引用

页码：90 / 100

页数：11

共 44 条

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