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目的观察荞麦花叶总黄酮(TFBFL)对心肌梗死大鼠的保护作用及机制。方法采用结扎左冠状动脉前降支建立大鼠心肌梗死模型,随机分为假手术对照组,模型组,TFBFL高、中、低剂量组(400,200,100mg·kg-1),麝香保心丸组(50 mg·kg-1)。模型复制后24 h各组灌胃给药,连续2周。比色法及ELISA法测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、白介素-6(IL-6)、白介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)、一氧化氮(NO)、内皮型一氧化氮合酶(eNOS)含量;硝基四氮唑蓝(NBT)染色测定心肌梗死面积。结果与模型组比较,TFBFL中、高剂量组大鼠心肌梗死面积缩小以及血清CK、LDH水平均降低(P<0.05,P<0.01);血清SOD、GSH-Px含量升高,MDA含量降低(P<0.05,P<0.01);IL-6、TNF-α水平降低,IL-10升高(P<0.05,P<0.01);NO、eNOS水平升高(P<0.05,P<0.01)。结论 TFBFL对心肌梗死大鼠有一定的保护作用,其作用机制可能与TFBFL的抗炎及抗氧化作用相关。
Objective To observe the protective effect of TFBFL on myocardial infarction in rats and its mechanism. Methods The model of myocardial infarction was established by ligation of left anterior descending coronary artery in rats. The rats were randomly divided into four groups: sham operation control group, model group, high, medium and low dose TFBFL groups (400, 200 and 100 mg · kg -1) 50 mg · kg-1). 24 h after model duplication, each group was given gavage for 2 weeks. The levels of creatine kinase (CK), lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde MDA, IL-6, IL-10, TNF-α, NO, eNOS ; Nitroblue tetrazolium blue (NBT) staining myocardial infarction area. Results Compared with model group, myocardial infarct size and serum CK and LDH levels in TFBFL medium and high dose groups were decreased (P <0.05, P <0.01), serum SOD, GSH-Px content and MDA content decreased (P <0.05, P <0.01). The levels of IL-6 and TNF-α decreased and the levels of IL-10 increased (P <0.05, P <0.01); the levels of NO and eNOS increased (P <0.05, P <0.01). Conclusion TFBFL can protect rats from myocardial infarction. Its mechanism may be related to the anti-inflammatory and anti-oxidation effects of TFBFL.