摘要
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 .
AIM: To investigate the preventive effects of QiDanTongMai Tablet (QDTMT) on mouse acute infarction and its possible mechanism. METHODS: SD mice were divided into control group, infarction group, QDTMT max dose group and QDTMT min dose group randomly. Different concentrations of QDTMT were administered to the four groups at same dosage twice a day for fourteen days before ligation. Coronary artery was ligated to establish the infarction animal model. Immunohistochemistry methods were used to detect the expression of VEGF and bFGF. RESULTS: Compared with that of the infarction group, the concentration of CPK and LDH decreased in all the QDTMT groups [LDH: (946±83) U·L -1 , (754±75) U·L -1 vs (1582±90) U·L -1 , ( P <0.01); CPK: (1135±69) U·L -1 , (960±39) U·L -1 vs (1513±47) U·L -1 , ( P < 0.01) ]. Infarction size in all the QDTMT groups decreased, and the left ventricular functions improved. QDTMT enhanced the expression of VEGF and bFGF. CONCLUSION: QiDanTongMai Tablet can prevent acute myocardial ischemia and enhance the expression of VEGF and bFGF.
出处
《第四军医大学学报》
北大核心
2003年第7期628-630,共3页
Journal of the Fourth Military Medical University
基金
陕西省攻关课题 (2 0 0 1k1 2 G7)