Carvacrol pretreatment attenuates myocardial oxidative stress and apoptosis following myocardial ischemia-reperfusion in mice.
- Author:
Xudong SONG
1
;
Aihua CHEN
;
Yingfeng LIU
;
Xian-Bao WANG
;
Yijun ZHOU
;
Lei LIU
;
Xiuli ZHANG
;
Lizi WANG
;
Pingzhen YANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antioxidants; pharmacology; Apoptosis; drug effects; Cardiotonic Agents; pharmacology; Male; Mice; Mice, Inbred C57BL; Monoterpenes; pharmacology; Myocardial Infarction; pathology; Myocardial Reperfusion Injury; metabolism; pathology; Myocytes, Cardiac; cytology; drug effects; Oxidative Stress; drug effects; Random Allocation
- From: Journal of Southern Medical University 2013;33(11):1624-1627
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of carvacrol pretreatment on myocardial ischemia-reperfusion (I/R) injury and its underlying mechanisms.
METHODSWild-type male C57 BL/6 mice were randomized into 5 groups (n=13), namely the sham-operated group, vehicle (DMSO in saline)+ I/R group, carvacrol (20 mg/kg) + I/R group, carvacrol (40 mg/kg) + I/R group, and carvacrol (60 mg/kg) + I/R group. The mouse models of myocardial I/R injury were established by a 45-min occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion for 2 h. Carvacrol or vehicle was administered intravenously 15 min before LAD occlusion. After reperfusion, the mice were examined for myocardial oxidative stress level and apoptosis rate.
RESULTSCompared with the vehicle group, the 3 carvacrol-pretreated groups showed significantly reduced myocardial infarct size, oxidative stress level and cardiac myocyte apoptosis rate (P<0.01).
CONCLUSIONCarvacrol can protect against myocardial I/R injury by inhibiting myocardial oxidative stress and apoptosis in mice.
