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目的 :研究芪丹通脉片 (QDTMT)对大鼠急性心肌缺血预防作用及其可能作用机制 .方法 :采用SD大鼠为研究对象 ,随机分为假手术组、损伤组、QDTMT大剂量组、QDTMT小剂量组 .各组均用生理盐水配置等体积药液灌胃 14d ,每日 2次 .冠脉结扎方法制造心肌梗死动物模型 ,采用心肌酶谱、心梗面积来检测模型 ,免疫组织化学染色检测缺血心肌血管内皮生长因子 (VEGF)、碱性成纤维细胞生长因子 (bFGF)的表达 .结果 :与模型组相比 ,用药组大鼠血清肌酸激酶同工酶含量降低乳酸脱氢酶 [LDH :(94 6± 83 )U·L-1,(75 4± 75 )U·L-1vs (15 82± 90 )U·L-1,(P <0 .0 1) ;CPK :(113 5± 69)U·L-1,(960± 3 9)U·L-1vs (15 13± 4 7)U·L-1,(P <0 .0 1) ],心肌梗死面积缩小 ,VEGF ,bFGF表达增加 .结论 :QDTMT能够预防急性心肌缺血 ;刺激心肌分泌VEGF ,bFGF可能是其重要的作用机制之一 .
Objective: To study the preventive effect of Qidan Tongmai Tablet (QDTMT) on acute myocardial ischemia in rats and its possible mechanism. Methods: SD rats were randomly divided into sham operation group, injury group, QDTMT high dose group. QDTMT low-dose group. Each group was treated with equal volume of saline solution for 14 days, twice daily. The animal model of myocardial infarction was made by coronary artery ligation and the model was detected by myocardial enzyme and myocardial infarction area. Chemical staining was used to detect the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in ischemic myocardium. Results: Compared with the model group, serum creatine kinase isoenzyme levels in the treatment group decreased lactate release. Hydrogenase [LDH: (94 6± 83) U·L-1, (75 4± 75) U·L-1 vs (15 82± 90) U·L-1, (P <0.01); CPK : (113 5± 69) U·L-1, (960± 39)U·L-1vs (15 13± 47)U·L-1, (P <0.01), myocardial infarct size Reduction, VEGF, bFGF expression increased. Conclusion: QDTMT can prevent acute myocardial ischemia; stimulation of myocardial secretion of VEGF, bFGF may be one of the important mechanisms.