左冠脉结扎致冠心病心肌缺血气虚证的病理机制研究  

Pathogenesis of qi deficiency syndrome of CHD myocardial ischemia induced by left coronary ligation

作　　者：李春[1] 王勇[1] 仇琪[2] 郭淑贞[1] 王伟[1] 

机构地区：[1]北京中医药大学基础医学院,北京100029 [2]北京安贞医院药剂科

出　　处：《北京中医药大学学报》2011年第9期605-608,共4页Journal of Beijing University of Traditional Chinese Medicine

基　　金：国家重点基础研究发展计划(973计划)项目(No.2003CB517105);国家科技重大专项(No.2009ZX09502-018);北京中医药大学校级课题(No.JYBZZ-XS007;2009JYBZZ-JS098)

摘　　要：目的探讨在冠心病心肌缺血不同病理阶段气虚证可能的病理机制及生物学基础。方法利用左冠状动脉结扎术制备冠心病心肌缺血气虚证的动物模型,全面动态采集四诊信息,术后采用酶联免疫法(Elisa)对模型组和假手术组动物血清的白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、肿瘤坏死因子(TNF-α)、基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)等指标进行检测。结果结合宏观体征与相关理化指标,确立术后4、45 d模型组大鼠均为气虚证。4 d时,与同期假手术组比较,TNF-αI、L-1I、L-6分别上升了5.52%1、6.45%、43.95%(P<0.05),MMP-2、MMP-9变化不显著(P>0.05);术后45 d,MMP-2、MMP-9分别上升了15.05%2、8.08%(P<0.05),而炎症因子浓度下降,如IL-6已恢复至正常水平(P>0.05)。结论该方法制备的冠心病心肌缺血模型,术后4 d炎症因子IL-1I、L-6、TNF-α等浓度升高,表明炎症反应主导了该阶段气虚证的病理机制;而45 d虽同为气虚证,但其表现主要为MMP-2、MMP-9等心肌重构、心功能低下等相关指标的改变,炎症因子浓度则恢复至正常水平。可见,气虚证在心肌缺血不同病理阶段主导病理机制不尽相同,研究其机制将为中医证候的生物学基础研究提供实验依据。Objective To discuss the possible pathogenesis and biological base of qi deficiency syndrome in different pathological stages of myocardial ischemia of coronary heart disease （CHD）. Methods The rat model of qi deficiency syndrome of CHD myocardial ischemia was established by applying left coronary ligation, and the information of TCM four examinations were collected generally and dynamically. The levels of interleukin-1 （IL-1）, interleukin-6 （IL-6）, tumor necrosis factor-α （TNF-α）, matrix metalloproteinase-2 （MMP-2） and matrix metalloproteinase-9 （MMP-9） were detected by using enzyme-linked immunosorbent assay in the model group and sham-operation group. Results After the operation for 4 days and 45 days, the qi deficiency syndrome was determined in model group from macroscopic signs and physicochemical indicators. After 4 days, the levels of TNF-α, IL-1 and IL-6 increased by, respectively, 5.52%, 16.45% and 43.95% （P 〈0. 05）, and the levels of MMP-2 and MMP-9 had no significant changes （ P 〉 0.05 ） in the model group compared with the sham-operation group in the same stage. After 45 days, the levels of MMP-2 and MMP-9 mcreaseci by, respecnvely, 15.05% and 28.08% （ P 〈 0.05 ） , while the concentration of inflammatory factors decreased and the level of IL-6 restored to normal （ P 〉 0.05）. Conclusion The levels of inflammatory factors including TNF-α, IL-1 and IL-6 increased in the model of CHD myocardial ischemia 4 days after the operation, which showed that the inflammatory reaction dominated the pathogenesis in this stage. After 45 days, the main manifestations of qi deficiency syndrome were the changes of MMP-2 and MMP-9, indexes related to myocardial remodeling and cardiac dysfunction, while the levels of inflammatory factors restored to normal. The leading pathogenesis of qi deficiency syndrome is different in the different pathological stages of myocardial ischemia. The study on the mechanism will provide experimental base for the biological and basic resea

关 键 词：心肌缺血 气虚证 炎症 心肌重构 大鼠 

分 类 号：R228[医药卫生—中医基础理论]