中医不同治法对心肌缺血再灌注损伤大鼠炎症相关细胞因子的影响

Effects of Different Chinese Medicine Treatments on Contents of Inflammation-related Cytokines in Rats with Ischemia-reperfusion Injury

目的观察中医不同治法对高脂血症心肌缺血再灌注损伤(MI/RI)大鼠炎症相关细胞因子含量的影响,探讨其对MI/RI的拮抗作用。方法 60只雄性SD大鼠随机分为假手术组、模型组、祛痰宽胸组、活血化瘀组及痰瘀同治组。除假手术组外,其余大鼠予高脂饲料喂养,采用可逆性冠脉左前降支结扎缺血30 min再灌注2 h复制MI/RI模型,检测再灌注后各组大鼠血清总胆固醇(CHO)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)以及细胞间黏附分子(ICAM)-1、肿瘤坏死因-α(TNF-α)、白细胞介素(IL)-10含量。结果与模型组比较,各治疗组血清CHO、TG、HDL-C、LDL-C含量降低(P<0.05,P<0.01),活血化瘀组血清ICAM-1含量降低(P<0.05),痰瘀同治组可抑制ICAM-1、TNF-α表达(P<0.05),祛痰宽胸组作用不显著(P>0.05)。结论活血化瘀法及痰瘀同治法对大鼠MI/RI有显著保护作用,其机理可能与调控血脂、抑制炎症因子表达,从而减轻炎症反应有关。

Objective To investigate the influence of different TCM treatments on contents of inflammationrelated cytokines of hyperlipidemia and myocardial ischemia-reperfusion injury（MI/RI） in rats,and discuss its mechanism of anti-inflammatory.Methods Sixty male rats were divided into sham-operated group,model group,removing phlegm and enlarging chest group,activating blood and dissolving stasis group,treating both phlegm and blood stasis group.All rats were fed with high-fat diet except for the sham-operated group.The model of MI/RI myocardium was reproduced by ligation of left descending artery for 30 min followed by releasing the ligation for 2 hours in rats.Serum contents of CHO,TG,HDL-C,LDL-C and ICAM-1,TNF-α,IL-10 were measured after myocardial reperfusion injury.Results Compared with model group,the level of different degrees of CHO,TG,HDL-L,LDL-L were lower in all groups treated by different TCM treatment（P〈0.01 or P〈0.05）.The contents of ICAM-1 was reduced in activating blood and dissolving stasis group（P〈0.05）,and the expression of ICAM-1,TNF-α were decreased in treating both phlegm and blood stasis group（P〈0.05）.While there was no significant difference between the removing phlegm and enlarging chest group and model group（P〈0.05）.Conclusion The activating blood and dissolving stasis method and treating both phlegm and blood stasis method can protect myocardium from MI/RI.The mechanism may be related to regulating hyperlipidemia and restraining the expression of inflammatory factors.