Effects and mechanism of TG6 on myocardial ischemia and reperfusion injury
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摘要: 目的 研究TG6对心肌缺血/再灌注损伤的保护作用及机制。 方法 采用整体大鼠心肌缺血/再灌注(I/R)实验,离体大鼠心脏低灌复灌实验和乳鼠心肌细胞缺氧/复氧损伤(H/R)实验等模型,以血清CK、LDH、T-SOD、MDA等为指标,研究TG6对心肌缺血再灌注损伤的保护作用。 结果 在整体大鼠心肌缺血再灌注损伤实验中,TG6显著减少I/R损伤后心肌梗死面积,减少血清中CK活力和MDA含量,减少LDH活力,增加T-SOD活力;在离体大鼠心脏低灌复灌实验中,TG6显著增加低灌复灌后心肌冠脉流量,减少心肌组织中MDA含量和CK、LDH外漏,提高心肌组织中T-SOD活力;在乳鼠心肌细胞H/R损伤实验中,TG6对正常生长条件下的细胞没有明显影响,提高Na2S2O4制备的心肌细胞H/R模型下细胞的存活率、降低细胞CK的释放率及细胞[Ca2+]i的含量。 结论 TG6对心肌I/R损伤有一定的保护作用。Abstract: Objective To investigate the protective effects and mechanism of TG6 on myocardial ischemia/reperfusion injury. Methods the protective effects of TG6 on myocardial ischemia/reperfusion was investigated by setting up models of ischemia and reperfusion of rats induced by ligating the left coronary anterior descending artery in vivo,isolated rat hearts through an improved Langendorff device, and hypoxia /reoxygenation injury of neonatal rat cardiomyocytes, and the serum CK,LDH,T-SOD, MDA were taken as research markers. Results TG6 significantly reduced the myocardial infarct size, decreased the activity of CK and the content of MDA in serum, reduced the activity of LDH, and increased the activity of T-SOD in vivo;TG6 obviously increased the coronary blood flow after low rate perfusion and reperfusion, decreased the content of MDA and the leakage of CK, LDH in myocardial tissue, elevated the activity of T-SOD in vitro of isolated rat hearts;TG6 had no effects on cells in normal growth condition, raised the viability of cardiomyocytes significantly, and reduced the rate of CK leakage and the content of [Ca2+]i obviously in Na2S2O4 treated cells in vitro of neonatal rat cardiomyocytes. Conclusion TG6 could effectively protect myocardial ischemia/reperfusion injury.
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Key words:
- NHEI /
- myocardial ischemia/reperfusion /
- coronary artery ligation /
- isolated heart perfusion /
- cardiomyocyte /
- H/R
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