摘要
目的观察含益气通络丹的大鼠血清对缺氧24h再给氧4h后新生乳鼠心肌细胞凋亡的抑制作用及其对心肌细胞乳酸脱氢酶(LDH)释放、一氧化氮(NO)生成和硫代巴比妥酸反应物质(TBARS)的影响。方法采用AnnexinV-PI双标记方法以流式细胞仪和ELISA法检测细胞凋亡,以紫外分光光度法测定LDH释放水平,采用改良Yu方法测定NO浓度,用Ohkawa法测定TBARS含量。结果心肌细胞缺氧再给氧后NO、TBARS水平升高,LDH释放增加。含益气通络丹的血清能显著抑制心肌细胞凋亡,抑制LDH释放,降低培养细胞上清液中NO和TBARS水平,其效应呈剂量依赖关系。结论益气通络丹具有抗缺氧再给氧心肌细胞凋亡作用,其机制与清除氧自由基和NO特性有关。
Objective To investigatethe inhibitoryeffectof Yiqitongluopelleton culturedneonatalrat cardiomyocyte apoptosisinducedby reoxygenationwithprecedinghypoxiaandobservethechangesin thelevelsof lactabledehydrogenase,nitricoxide(NO)andthiobarbituricacid-reactivesubstances(TBARS)in theinoculum.Methods The neonatalrat cardiomyocyteswereobtainedto establishmodelsof reoxygenationfollowinghypoxia,andsubsequentlytreatedwiththe serumisolatedfrom Yiqitongluopellet-fedWistarratsadministeredbeforeannexinV-PIlabeling.Flowcytometryand enzyme-linkedimmunosorbentassaywereperformedfor cellularapoptosisassessment.The concentrationof LDHin the inoculumwasmeasuredwithspectrophotometer,andimprovedYu methodandOhkawamethodwereemployedto determine NO and TBARSlevels,respectively.Results Yiqishuluopelletratserumsignificantlyinhibitedthecardiomyoctesfrom apoptosisinducedby reoxygenationwithprecedinghypoxia,and the elevatedNO,LDH and TBARSlevelsdue to reoxygenationintheinoculumwerebroughtdownby themedication-containingserum.Conclusion Yiqitongluocaninhibite cardiomyocyteapoptosisinducedby reoxygenationfollowinghypoxiaby themechanisminvolvingtheeliminationof oxygen freeradicalsandNOproductionregulation.
出处
《第一军医大学学报》
CSCD
北大核心
2001年第10期743-745,共3页
Journal of First Military Medical University
基金
国家自然科学基金(39300178)
广东省自然科学基金(95056719)
关键词
供氧
通络
脱噬作用
心肌再灌注
益气通络丹
reinforcingagent
anoxia
dredgingcollaterals
apoptosis
myocardium
myocardialreperfusioninjury
