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目的:研究槲寄生黄酮苷(VCFG)对大鼠离体心肌缺血再灌注损伤(MIRI)的保护作用。方法:采用离体langendorff法缺血再灌注模型,停灌30min,复灌40min,对照组持续灌注90min。实验后检测心肌组织中肌酸激酶(CK)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、诱导型一氧化氮合酶(NOS)、总一氧化氮合酶活性(tNOS)及一氧化氮(NO)含量。结果:槲寄生高剂量组(0.3g.kg-1)能显著降低离体缺血再灌注后CK水平(P<0.01),升高SOD(P<0.01)、GSH-PX(P<0.01)和NOS活性(P<0.01),并使NO含量明显增高(P<0.01,P<0.05)。且VCFG高剂量组作用强度与地奥心血康(DK)相似。结论:VCFG有较好的抗心肌缺血再灌注损伤作用。其机制可能与抗氧自由基损伤有关。
Objective: To study the protective effect of mistletoe flavonoid glycoside (VCFG) on isolated rat myocardial ischemia-reperfusion injury (MIRI). Methods: The model of ischemia-reperfusion was established in vitro with langendorff method. The rats were infused for 30 minutes and reperfusion for 40 minutes. The control group was infused for 90 minutes. The levels of creatine kinase (CK), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), inducible nitric oxide synthase (NOS) Nitrogen synthase activity (tNOS) and nitric oxide (NO) content. Results: The high dose of mistletoe group (0.3g.kg-1) significantly reduced the level of CK (P <0.01), the level of SOD (P <0.01) And NOS activity (P <0.01), and NO content was significantly increased (P <0.01, P <0.05). The intensity of VCFG high-dose group was similar to that of DI (DX). Conclusion: VCFG has good anti-ischemic and reperfusion injury. The mechanism may be related to antioxidant free radical damage.