摘要
目的探讨急性心肌梗死发生后再予以FNS是否对缺血心肌具有保护作用。方法将大鼠随机分为4组:①AMI组,仅结扎左冠状动脉前降支(LAD);②FNS组,预先LAD结扎后予以FNS1h;③小脑顶核毁损组(FNL组),预先毁损小脑顶核5d后再行LAD结扎,随后FNS1h;④假手术组。LAD结扎后24h,应用RT-PCR法测定左心室梗死区IL-1β、IL-6、TNF-αmRNA表达;应用化学法测定心肌梗死面积,以及心肌组织丙二醛(MDA)含量、总抗氧化能力(TAOC)、超氧化物岐化酶(SOD)活性。结果与AMI组比较,FNS组心肌梗死面积显著减少(P<0.05),梗死区IL-1β、IL-6、TNF-αmRNA表达亦显著减少(P<0.05)。与假手术组比较,AMI组和FNL组梗死心肌MDA含量明显增加(P<0.01),而TAOC及SOD活性显著下降(P<0.01);与AMI组比较,FNS组大鼠梗死心肌MDA含量明显减少(P<0.05),TAOC及SOD活性显著增加(P<0.05)。FNL组与AMI组间以上指标比较无统计学差异(P>0.05)。结论 FNS可减少大鼠心肌梗死后的心肌损伤;这一保护作用机制,可能与其下调心肌梗死区IL-1β、IL-6、TNF-αmRNA表达,调节氧化-抗氧化成分的平衡有关。
Objective Increasing evidence suggests that fastigial nucleus（FN）stimulation can provide tissue protection from ischemic injury.Previous studies showed that FN stimulation（FNS）decreased the volume of cerebral infarction.Our previous study discovered that FNS before acute myocardial infarction（AMI）had protective effects on ischemic myocardium in rats,including reducing myocardial infarct size.However,the critical question whether FNS after AMI can have the same protective effects on ischemic myocardium remains unanswered.This study investigated this question.Methods Rats were divided into four groups：sham operation group,AMI group（induced by ligating the left anterior descending artery）,FNS group（receiving FNS 1 h after AMI）,FN lesion（FNL）group（performed with bilateral FN lesion for 5 d before the nucleus was electrically stimulated and AMI was induced）.At 24 h after AMI,changes of interleukin-1bata（IL-1β）,interleukin 6（IL-6）,tumor necrosis factor-alpha（TNF-α）mRNA expression were measured in the infracted zone with RT-PCR method,and the myocardial infarction size,the content of malondialdehyde（MDA）,total anti-oxidative capability（TAOC）and superoxide dismutase（SOD）activity were determined in the infracted zone with chemical method.Results Compared with AMI group,infarct sizes and IL-1β,IL-6,TNF-α mRNA expression in FNS group were significantly reduced（P〈0.05）.Compared with sham-operation group,the contents of MDA significantly increased,while activities of TAOC and SOD significantly decreased in AMI and FNL groups（P〈0.01）.Compared with AMI group,the contents of MDA significantly decreased,and activities of TAOC and SOD increased in the infarct zones in FNS group（P〈0.05）.There was no significant difference between FNL group and AMI group for all the measurements（P〈0.05）.Conclusion FNS could reduce myocardial damage after AMI.The mechanism of the protective effect may involve in the modulation of IL-1β,IL-6,TNF-α mRNA expression and oxidative and anti-oxidative balance in the infarct zones.
出处
《山西医科大学学报》
CAS
2010年第9期764-770,共7页
Journal of Shanxi Medical University
基金
国家自然科学基金资助项目(30571780)
中国博士后基金资助项目(KLF151016)
关键词
小脑顶核
电刺激
心肌梗死
炎性细胞因子
抗氧化
fastigial nucleus
electrical stimulation
myocardial infarction
inflammatory cytokine
antioxidant
