龙血竭对实验树鼩体外心肌缺血再灌注模型的影响

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目的:基于树鼩体外心肌缺血再灌注模型,探讨龙血竭对心肌缺血再灌注损伤的作用。方法:实验树齣随机分为空白组,模型组,溶媒组和龙血竭低、中、高质量浓度组(0.25,0.5,1.0 g·L~(-1)),采用Langendorff离体心脏灌流系統建立实验树駒心肌缺血后再灌注模型,灌注结束后立即取下心脏,-20℃冷冻。酶标法测定丙氨酸氨基转移酶(ALT),天门冬氨酸氨基转移酶(AST)和乳酸脱氢酶(LDH),免疫抑制法测定肌酸激酶MB(CK-MB),黄嘌呤氧化酶法测定超氧物歧化酶(SOD),硫代巴比妥酸染色法测定丙二醛(MDA),2,3,5-氯化三苯基四唑染色法(2,3,5-triphenyltrazolium chloride,TTC)测定切片梗死面积,末端脱氧核背酸转移酶介导的dUTP缺口末端标记测定法[terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling,TUNEL]检测凋亡率。结果:龙血竭药物再灌注后,灌注液及组织中AST,ALT,CK-MB,JLDH等指标显著下降,SOD活性显著增加,心肌梗死面积和TUNEL凋亡率显著下降(P<0.05)。结论:用龙血竭进行再灌注,能够抑制过多氧自由基的产生,减少心肌梗死面积和細胞凋亡,具有抗心肌缺血再灌注损伤作用。 OBJECTIVE: To investigate the effect of dragon’s blood on myocardium ischemia-reperfusion injury based on the model of myocardial ischemia-reperfusion in tree shrew. Methods: The experimental groups were randomly divided into blank group, model group, vehicle group and low, medium and high concentration of dragon’s blood group (0.25,0.5,1.0 g · L -1), Langendorff isolated cardiac perfusion The experimental model of Myocardial Ischemia and Reperfusion was set up. The heart was removed immediately after perfusion and frozen at -20 ℃. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were measured by enzyme-linked immunosorbent assay. Creatine kinase MB (CK-MB) The activity of superoxide dismutase (SOD) was measured by enzymatic method and the content of malondialdehyde (MDA) was measured by thiobarbituric acid staining. The 2,3,5- (TdT) -mediated dUTP nick end labeling (TUNEL) was used to detect the apoptotic rate of the infarcted area. The apoptotic rate was detected by TdT-mediated dUTP nick end labeling (TUNEL). Results: The indexes of AST, ALT, CK-MB and JLDH in perfusate and tissue were significantly decreased, the activity of SOD increased significantly, the area of ​​myocardial infarction and the apoptosis rate of TUNEL were significantly decreased (P <0.05). Conclusion: DRG reperfusion can inhibit the production of excessive oxygen free radicals, reduce myocardial infarct size and apoptosis, and have anti-myocardial ischemia-reperfusion injury.
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