摘要
目的探讨大黄素(emodin)对大鼠离体心脏缺血/再灌注损伤的保护作用及其机制。方法健康成年♂SD大鼠24只,随机分为4组:对照组(control)、大黄素组(emodin)、大黄素+格列本脲组(glibenclamide,Gli)和大黄素+5-HD组(5-hydroxydecanoate,5-HD)。通过Langendorff离体心脏灌流技术建立心肌缺血/再灌注模型和描记左室功能;紫外分光光度法测定冠脉流出液中LDH含量及心肌组织中SOD活性和MDA含量;TTC法测定心肌梗死面积。结果 (1)大黄素可明显改善缺血/再灌注后大鼠离体心脏左心室发展压(left ventricular develop pressure,LVDP)、左心室压力最大变化速率(maximal positive and negative velocity of left ventricular pressure,±LVdp/dt max)、左心室舒张末压(left ventricular end-diastolic pressure,LVEDP)和冠脉流量(coronary flow,CF)的恢复;降低冠脉流出液中LDH含量;减少心肌梗死面积;升高心肌组织中SOD活性,减少MDA含量;(2)大黄素对离体心脏缺血/再灌注损伤的保护作用可被非特异性ATP敏感钾通道拮抗剂Gli和线粒体膜ATP敏感钾通道拮抗剂5-HD所取消。结论大黄素可改善离体大鼠心脏缺血/再灌注损伤,此作用可能通过增强心肌的抗氧化能力、激活开放细胞膜与线粒体膜ATP敏感钾通道所实现。
Aim To investigate the protective effect of emodin on the ischemia/reperfusion injury and the un- derlying mechanism in isolated rat heart. Methods Adult male Sprague-Dawley rats,weighing 270 - 320g, were randomly divided into four groups： control, emo- din, emodin ＋ glibenelamide （ Gli ） and Emodin ＋ 5- hydroxydecanoate （ 5-HD ） groups. Left ventricular function of rat was recorded by using Langendorff tech- nique before and after myocardial ischemia/reperfusion （I/R）. The activity of myocardial superoxide dis- mutase （SOD） and the contents of myocardial malond- ialdehyde （ MDA）, as well as activity of lactate dehy- drogenase （LDH） in coronary effluent were spectro- photometrically assayed. The rat hearts were dyed with TTC and the infarct size was measured with image anal- ysis software. Results （1） Emodin improved the re- covery of LVDP, ± LVdp/dtmax, LVEDP and CF afterI/R, and reduced the LDH in coronary effluent after I/ R. Emodin also reduced the infarct size after I/R. Furthermore, emodin incresed the activity of SOD and decreased the content of MDA in myocardium. （2） The cardiac protection of emodin against I/R injury in isolated heart was abolished by antagonist of ATP sen- sitive potassium channel glibenclamide and antagonist of ATP sensitive potassium channel in mitochondrial membrane 5-HD. Conclusion Emodin protects heart against I/R injury in isolated rat heart, which may be accomplished by increasing the antioxidant ability of myocardium, activating and opening ATP sensitive po- tassium channel in both cell membrane and mitochon- drial membrane.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2013年第12期1721-1725,共5页
Chinese Pharmacological Bulletin
基金
河北省科技厅课题(No 122777116)
