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

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(nuclear factor—kappa B，NF—κB)信号途径及心肌细胞间隙连接蛋白Cx43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—κB p65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Cx43表达。结果模型组大鼠心肌梗死面积及梗死区重量、NF-κB p65表达、血清中TNF-α及ICAM—1含量明显升高(P<0．05)；心肌连接蛋白Cx43大量降解。SSTG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<0．05)；NF—κB p65表达及Cx43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，Cx43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Cx43的降解，减小心肌梗死面积及重量。

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

OBJECTIVE: To investigate the effects of Shuangshen Tongguan Recipe (SSTG) on myocardial nuclear factor-kappa B (NF-kappaB) 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. METHODS: Model 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-kappaB p65 in myocardial tissue and Cx43 were determined by immunohistochemical method, contents of serum tumor necrosis factor-alpha(TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) were measured by ABC-ELISA. RESULTS: The myocardial infarcted size and weight, expression of NF-kappaB p65, contents of serum TNF-alpha 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). CONCLUSION: Serious myocardial infarction occurs after ischemia/reperfusion injury, combined with NF-kappaB signal pathway activation and severe Cx43 degradation. SSTG could inhibit the activation of NF-kappaB, the over-excretion of TNF-alpha and ICAM-1 in serum, and the degradation of Cx43 to decrease the myocardial infarcted size and weight.