摘要
目的探讨曲美他嗪对缺血/再灌注(I/R)心肌细胞凋亡的影响及其机制。方法30只雄性新西兰白兔随机分入假手术组、对照组和治疗组,每组10只。治疗组在普通饲料喂养基础上,每只每日给予曲美他嗪2mg/kg灌胃。14d后制备I/R模型。采用末端脱氧核甘酸转换酶介导的生物素平移缺口末端标记技术(TUNEL)检测心肌细胞凋亡,用黄嘌呤氧化酶法测定血清超氧化物歧化酶总活力(T-SOD)和硫代巴比妥酸法测定血清丙二醛(MDA)浓度。结果与假手术组比较,对照组心肌细胞凋亡显著增加,T-SOD下降,MDA浓度增加,治疗组T-SOD及MBA与假于术组比较无明显差异,但心肌细胞凋亡明显高于假手术组;与对照组相比,治疗组凋亡指数明显减少,T-SOD显著增加,血清MDA浓度明显降低。结论新西兰兔在持续缺血后再灌注心肌细胞出现明显的凋亡现象,体内抗氧化酶活力下降,曲美他嗪预治疗对缺血后再灌注诱导的心肌细胞凋亡具有一定的抑制作用,曲美他嗪的细胞保护作用可能通过其抗氧化作用机制。
Objective To investigate the effect of trimetazidine on ischemia/reperfusion（I/R）-mediated cardiomyocyte apoptosis and its mechanisms.Methods Thirty New Zealand white male rabbits was randomly dividedd into 3 groups：sham,control and pretrestment （ n = 10, respectively）. The pretreatment was additionally fed daily with trimetazidine （2 mg· kg^- 1· d^- 1 ）. 14 days later, the I/R model was established. The apoptotic cardiomyocytes were assessed by terinal deoxynucleotidyl transferase-mediated dUTP nick end labelling （TUNEL）. The total activity of serum superoxide dismutase （T-SOD） were determined by the method of xanthine oxidase,and the contents of serum rnalondialdehyde （MDA） were checked by colorimetry. Results Compared with the sham, I/R alone induced markedly increasing apoptosis of cardiomyocytes,T-SOD was significantly depressed and the serum MDA was markedly increased. There are no difference between the pretreatment and the sham, but the apoptotic index in the pretreatment was still higher than that in the sham. Compared with the control, the apoptotic index and MDA in the treatment was markedly decreased, and T-SOD was significantly increased.Conelusion These data suggest that I/R markedly induces cardiomyocyte apoptosis and depresses the activity of antioxidase. Trimetazidine may effectively prevent cardiomyocyte apoptosis from postischemia reperfusion via antioxidant mechanism.
出处
《广西医学》
CAS
2006年第4期481-484,共4页
Guangxi Medical Journal
基金
广西壮族自治区"新世纪十百千人才工程"专项资助资金项目(批准号:20012112)
关键词
缺血/再灌注
曲美他嗪
心肌细胞
凋亡
Ischemia/reperfusion
Cardiomyocyte
Apoptosis
Trimetazidine
