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 .0 5 )。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 .0 5 )。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 )
Objective: To observe the effects of SSTG on in fa rction size and tumor necrosis factor-α(TNF-α), intercellular adhesion mo lecular-1 (ICAM-1)levels in serum during reperfusion injury of acute myocar dial ischemia. Method: Anterior descending branch of coronary artery was ligated and released to create myocardial ischemia-reperfusion injur y . The size and weight of infarction area and the contents of TNF-α, ICAM-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-α, ICA M-1 in serum were significantly increased compared with the normal group and we re obviously decreased after being treated with SSTG. Conclusion: Ischemia-reperfusion stimulated the secretion of TNF-α and ICAM-1, whic h play an important role in ischemia-reperfusion injury. SSTG might protect myo cardium from ischemia-reperfusion injury by suppressing over-secretion of TNF -α and ICAM-1 and reducing the size and weight of infarction area. [
出处
《中国中药杂志》
CAS
CSCD
北大核心
2004年第11期1073-1075,共3页
China Journal of Chinese Materia Medica
基金
国家自然科学基金资助项目 (3 0 17114 9)