双参通冠方对急性心肌缺血再灌注模型核因子-κB信号途径及细胞间隙连接通讯的影响

Effect of Shuangshen Tongguan Recipe on Nuclear Factor-kappa B Signal Pathway and Myocardial Junction-Mediated Intercellular Communication in Acute Myocardial Ischemia/Reperfusion Injured Model Rats

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中文关键词: 双参通冠方缺血再灌注损伤核因子-κB 信号途径肿瘤坏死因子细胞间黏附分子-1 细胞间通讯连接蛋白43

英文关键词:Shuangshen Tongguan Recipe ischemia/reperfusion injury nuclear factor-κ B signal pathway tumor necrosis factor-α intercellular adhesion molecule-1 intercellular communication connexin 43

基金项目:国家“8 63”计划课题 (No .2 0 0 4AA2 2 381 2 )

作者	单位
刘建勋	中国中医研究院西苑医院实验研究中心北京100091
韩笑	中国中医研究院西苑医院实验研究中心北京100091
马晓斌	中国中医研究院西苑医院实验研究中心北京100091
王杨慧	中国中医研究院西苑医院实验研究中心北京100091

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中文摘要:

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面积及重量 ,心肌核因子 κB(nuclearfactor- kappaB ,NF-κB)信号途径及心肌细胞间隙连接蛋白Cx4 3的影响。方法用冠状动脉结扎 /放松法复制大鼠心肌缺血再灌注损伤模型 ,N-BT染色法测量心肌梗死范围 ;免疫组织化学法检测心肌组织NF-κBp6 5表达 ;双抗体夹心ABC-ELISA法测定各组血清肿瘤坏死因子 (TNF α)和细胞间黏附分子- 1(ICAM-1)含量 ;免疫组织化学法测定心肌细胞通讯间隙连接蛋白Cx4 3表达。结果模型组大鼠心肌梗死面积及梗死区重量、NF-κBp6 5表达、血清中TNF-α及ICAM-1含量明显升高 (P <0.0 5 ) ;心肌连接蛋白Cx4 3大量降解。SSTG处理后心肌梗死面积及重量减轻 ;血清中TNF α、ICAM 1水平下调 (P <0 0 5 ) ;NF κBp6 5表达及Cx4 3降解抑制。结论缺血再灌注时 ,心肌梗死严重 ,NF κB信号途径可被激活 ,Cx4 3降解严重。SSTG能抑制NF-κB的活化 ,抑制血清中TNF-α、ICAM-1的过量分泌和抑制Cx4 3的降解 ,减小心肌梗死面积及重量

英文摘要:

investigate the effects of Shuangshen Tongguan Recipe (SSTG) on myocardial nuclear factor-kappa B (NF-κB) signal pathway, expression of myocardial junction intercellular communication (MJIC) connexin 43 (Cx43), and infarcted myocardial size and weight of the rats’ heart after acute myocardial ischemia/reperfusion (I/R) damage. MethodsModel rat of I/R injury was established by coronary arterial ligating/releasing. The infarcted myocardial size and weight were determined by N-BT staining, expression of NF-κB p65 in myocardial tissue and Cx43 were determined by immunohistochemical method, contents of serum tumor necrosis factor-α(TNF-α) and intercellular adhesion molecule-1 (ICAM-1) were measured by ABC-ELISA. ResultsThe myocardial infarcted size and weight, expression of NF-κB p65, contents of serum TNF-α and ICAM-1 of I/R injured rats in the model group were significantly increased (P<0.05), while Cx43 degraded markedly after modeling. These changes were restored after treated with SSTG (P<0.05). ConclusionSerious myocardial infarction occurs after ischemia/reperfusion injury, combined with NF-KB signal pathway activation and severe Cx43 degradation. SSTG could inhibit the activation of NF-κB, the over-excretion of TNF-α and ICAM-1 in serum, and the degradation of Cx43 to decrease the myocardial infarcted size and weight.

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