香芹酚预处理减轻小鼠心肌缺血再灌注时氧化应激及细胞凋亡

摘要

目的：探索香芹酚（CAR）对小鼠心肌缺血再灌注损伤的作用及其相关机制。方法结扎雄性C57 BL/6小鼠冠状动脉左前降支45 min后解除结扎线构建急性心肌缺血再灌注（I-R）损伤模型。动物被随机分为5组：假手术组（n=13）、Vehicle组（DMSO in saline+I-R组）（n=13）、CAR组（CAR+I-R组）：分为20、40及60 mg/kg组（每组n=13）。CAR于缺血前15 min给药。缺血45 min再灌注2 h后检测心肌组织氧化应激水平及细胞凋亡率。结果同Vehicle组相比，CAR组心肌缺血再灌注后心肌梗死面积、氧化应激水平及细胞凋亡率显著降低（P<0.05）Vehicle组及CAR组DCFDA强度分别为（158.21±6.43）%及（123.47±9.82）%。Vehicle组及CAR组Mn-SOD活性分别为0.67±0.16及1.12±0.17 U/mg protein。Vehicle组及CAR组过氧化氢酶活性分别为0.14±0.09及0.63±0.07 U/mg protein。结论 CAR可通过降低氧化应激水平及心肌细胞凋亡率缓解小鼠心肌缺血再灌注损伤。%Objective To investigate the effect of carvacrol pretreatment on myocardial ischemia-reperfusion (I/R) injury and its underlying mechanisms. Methods Wild-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. Results Compared 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). Conclusion Carvacrol can protect against myocardial I/R injury by inhibiting myocardial oxidative stress and apoptosis in mice.