摘要
目的:研究阿魏酸钠(SF)在心肌缺血/再灌注损伤中的保护作用机制。方法:40只SD大鼠随机分为假手术组、模型组和SF组(结扎后5min注射SF),采用左冠状动脉前降支结扎法制备大鼠心肌缺血/再灌注模型,以免疫酶标法检测大鼠血清内缺血/再灌注肌酸激酶同工酶(CK-MB)和诱导型一氧化氮合酶(iNOS)的含量;以TUNEL(FITC)法检测心肌细胞的凋亡指数;并用半定量PCR的方法检测心肌组织内Bcl-2蛋白的表达。结果:与模型组相比,SF能降低心肌缺血/再灌注后CKMB及iNOS的含量(P<0.05),降低缺血部位凋亡心肌细胞的数量(P<0.05),促进Bcl-2蛋白的表达。结论:与其他报道一致,SF处理后,心肌细胞抗氧化能力增强;除此之外,心肌细胞内凋亡调节蛋白Bcl-2的表达增加,缺血局部凋亡细胞数量降低,从而减轻心肌缺血/再灌注部位的损伤,维持正常的心肌功能。本研究提示,心肌缺血/再灌注前使用SF的治疗,将有助于保护缺血心肌和心肌功能的恢复。
Objective：To evaluate the protected effects of sodium ferulate on myocardium with ischemia reperfusion infury.Method：Forty SD rats were randomly divided into 3groups,sham operation group（S group）,ischemia-reperfusion group（I/R group）,sodium ferulate group（sodium ferulate treatment followed by ischemia-reperfusion,SF group）.Myocardial ischemia reperfusion model was established by ligating left anterior descending coronary artery.The contents of creatine kinase MB（CKMB）,inducible nitric oxide synthase（iNOS）in serum were determined by ELISA.The protein expression of Bcl-2was detected by RTPCR.TUNEL was used to detect the myocardium apoptosis.Result：Compared with the I/R group,SF group show decreased concentration of CKMB and iNOS（P〈0.05）.The SF group rats showed less apoptosis myocardium cells than I/R group rats（P〈0.05）.The level of Bcl-2expression were increased in SF group rat.Conclusion：As the reports,the sodium ferulate can promote the myocardium antioxidant capacity.And furthermore it can inhibit myocardium apoptosis induced by the ischemic reperfusion injury,probably as a result of the increased expression of Bcl-2protein.
出处
《临床急诊杂志》
CAS
2017年第1期35-37,共3页
Journal of Clinical Emergency
基金
武汉市卫计委项目(No:WX09Z02)
关键词
阿魏酸钠
心肌
缺血/再灌注
细胞凋亡
sodium ferulate
myocardium
ischaemia reperfusion injury
apoptosis
