黑木耳多糖对抗离体心脏缺血/再灌注损伤的研究

目的:探讨黑木耳多糖(AAP)对离体大鼠心脏缺血/再灌注(I/R)损伤的防护作用及其机制。方法:健康雄性SD大鼠灌胃黑木耳多糖(50,100,200mg/(kg.d))4周后,采用离体心脏Langendorff灌流方法,全心停灌30min,复灌120min建立I/R模型。测定左心室动力学指标和再灌注各时间点冠脉流出液中乳酸脱氢酶(LDH)含量;实验结束测定心肌组织甲月赞(formazan)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性的变化。结果:与单纯I/R组相比,AAP预处理明显提高心肌细胞的formazan含量,降低再灌注期间冠脉流出液中LDH含量,明显增强左室发展压、左心室内压最大上升速率和心率与发展压乘积的恢复,缓解冠脉流量的减少;高剂量AAP改善I/R心肌功能的作用要好于丹参预处理(4ml/(kg.d),gastricperfusion)组。中剂量AAP(100mg/(kg.d))预处理4周后明显抑制I/R心肌MDA的增加和SOD活性的减弱(P0.01),其效果要好于丹参阳性对照组。结论:在大鼠离体心脏灌流模型上,黑木耳多糖预处理具有抗心脏I/R损伤的作用,这种保护作用可能与其增加心肌SOD活性,减少脂质过氧化损伤有关。

Auricularia auricular polysaccharide protects myocardium against ischemia/reperfusion injury

Objective：To determine whether auricularia auricular polysaccharide （AAP） protects heart against ischemia/reperfusion （I/R） injury and its underlying mechanisms.Methods：Male Sprague-Dawley rats,pretreated with AAP （50,100,200 mg/（kg·d）,gastric perfusion） for 4 weeks,were used for Langendorff isolated heart perfusion.The hearts were subjected to global ischemia for 30 min followed by 120 min of reperfusion and the left ventricular hemodynamic parameters were measured.Formazan,a product of 2,3,5-triphenyl-tetrazolium chloride （TTC）,which is proportional to myocardial viability,was measured at 490 nm,and the level of lactate dehydrogenase （LDH） in the coronary effluent was measured to evaluate the cardiac injury.The cardiac malondialdehyde （MDA）,a product of lipid peroxidation,and superoxide dismutase （SOD） activity were determined after myocardial I/R.Results：The pretreatment with AAP at 50,100,200/（kg·d） for 4 weeks before I/R increased myocardial formazan content,reduced LDH release,improved the recovery of the left ventficular developed pressure,maximal rise rate of left ventricular pressure,and rate pressure product （left ventricular developed pressure multiplied by heart rate） and attenuated the decrease of coronary flow during reperfusion.The cardiac protective effect of high dose AAP was more potent than that of compound radix salviae miltiorrhizae （CRSM,4 ml/（kg·d）,gastric perfusion for 4 weeks）.Pretreatment with AAP （100 mg/（kg·d）） markedly inhibited the increase of MDA level and the decrease of SOD activity induced by I/R in myocardium.Conclusion：The findings indicate that in the isolated rat heart,AAP protects myocardium against ischemia/reperfusion injury via enhancing the activity of SOD and reducing lipid peroxidation in heart.