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双参通冠方对急性心肌缺血再灌注损伤时TNF-α,ICAM-1的影响
引用本文:韩笑,刘建勋马晓斌,王杨慧. 双参通冠方对急性心肌缺血再灌注损伤时TNF-α,ICAM-1的影响[J]. 中国中药杂志, 2004, 29(11): 1073-1075
作者姓名:韩笑  刘建勋马晓斌  王杨慧
作者单位:中国中医研究院,西苑医院,实验研究中心,北京,100091
摘    要:目的 :观察双参通冠方 (SSTG)对急性心肌缺血再灌注损伤动物模型心肌梗死范围及血清中肿瘤坏死因子 (TNF-α)、细胞间黏附分子-1(ICAM-1)含量的影响。方法 :冠状动脉结扎 /放松法复制大鼠心肌缺血再灌注损伤模型 ,分为正常组 (假手术组 )、模型组、SSTG高、低剂量组 ,N-BT染色法测量心肌梗死范围 ,双抗体夹心ABC-ELISA法测定各组血清中TNF-α ,ICAM-1的含量。结果 :缺血再灌注损伤模型组心肌梗死面积及梗死区重量明显异常 ,血清中TNF-α ,ICAM-1含量增高 (P<0.05 )。SSTG处理后心肌梗死面积缩小、梗死重量减轻、梗死 /心室 (心脏 )百分比降低 ,血清中TNF-α ,ICAM-1含量下调 (P<0.05 )。结论 :受缺血再灌注刺激时血清中TNF-α,ICAM-1含量增加 ,双参通冠方可能通过抑制TNF-α ,ICAM-1的过量分泌而保护受损心肌 ,表现为心肌梗死面积减小、梗死区重量减轻及梗死 /心室 (心脏 )百分比降低。

关 键 词:缺血再灌注损伤  肿瘤坏死因子  细胞间黏附分子-1
文章编号:1001-5302(2004)11-1073-03
收稿时间:2003-12-30

Effects of Shuangshen tongguan(SSTG) on TNF-α, ICAM-1 during myocardial ischemia-reperfusion injury
HAN Xiao;LIU Jian-xun;MA Xiao-bin;WANG Yang-hui. Effects of Shuangshen tongguan(SSTG) on TNF-α, ICAM-1 during myocardial ischemia-reperfusion injury[J]. China Journal of Chinese Materia Medica, 2004, 29(11): 1073-1075
Authors:HAN Xiao  LIU Jian-xun  MA Xiao-bin  WANG Yang-hui
Affiliation:Xiyuan Hospital, China Academy of Traditional Chinese Medicine, Beijing 100091, China.
Abstract:OBJECTIVE: To observe the effects of SSTG on infarction size and tumor necrosis factor-alpha (TNF-alpha), intercellular adhesion molecular-1 (ICAM-1) levels in serum during reperfusion injury of acute myocardial ischemia. METHOD: Anterior descending branch of coronary artery was ligated and released to create myocardial ischemia-reperfusion injury. The size and weight of infarction area and the contents of TNF-alpha, IGAM-1 in serum were assayed by N-BT staining and ELISA respectively. RESULT: The size and weight of infarct area and the contents of TNF-alpha, ICAM-1 in serum were significantly increased compared with the normal group and were obviously decreased after being treated with SSIG. CONCLUSION: Ischemia-reperfusion stimulated the secretion of TNF-alpha and ICAM-1, which play an important role in ischemia-reperfusion injury. SSTG might protect myocardium from ischemia-reperfusion injury by suppressing over-secretion of TNF-alpha and ICAM-1 and reducing the size and weight of infarction area.
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