肿瘤坏死因子在冠心病心肌缺血模型证候演变中的表达

Experimental study on role of TNF-α in syndromes development of myocardial ischemia model

目的:探讨肿瘤坏死因子(TNF-α)在冠心病心肌缺血动物模型由"气虚血瘀证"向"气虚证"演变过程中的作用。方法:采用动态宏观体征与理化指标相结合的方法进行模型动物证候属性判定,利用酶联免疫法(ELISA)检测炎症相关因子TNF-α,白介素-1(IL-1),白介素-6(IL-6),通过心脏超声检测心肌肥厚与心功能相关指标。结果:模型动物在术后7-60d表现为"气虚血瘀证→气虚证"的证候演变过程,TNF-α在整个疾病发展过程中持续高表达。在气虚血瘀证时,TNF-α的升高伴随着炎症因子IL-1、IL-6的升高;在气虚证时,除TNF-α外,炎症反应基本消退,而以心肌肥厚为主的心功能下降为该阶段的主要表现。结论:同一疾病的不同证候内在主导病理机制不尽相同。在冠心病心肌缺血过程中,TNF-α前期介导了炎症反应的发生,后期可能介导了心肌肥厚与心室重构的病理变化,由此推测,TNF-α效能的转移可能介导了气虚血瘀证向气虚证的演变。

Objective：To explore the role of tumor necrosis factor（TNF-α） in the syndrome development from ＇blood stasis and qi deficiency＇ to ＇qi deficiency＇ with animal models of myocardial ischemia.Methods：Combining dynamic symptoms with biochemical indicators to evaluate syndrome.ELISA was applied to detect inflammation factors such as TNF-α,IL-1,IL-6,and cardiac ultrasound was used to examine cardiac function and cardiac hypertrophy.Results：7-60 days after the surgery,development of the syndrome transformed from ＇blood stasis and qi deficiency＇ to ＇qi deficiency＇,the TNF-α was over-expression and last all over the pathological progress.At the stage of blood stasis and qi deficiency,the concentration of TNF-α was up-regulated as the increase of inflammatory cytokines IL-1 and IL-6,however,during the stage of qi deficiency,the inflammatory down-regulated to normal level.But it mainly performed as cardiac hypertrophy and heart dysfunction.Conclusion：Different syndrome had different pathology in same disease.TNF-α first mediates the inflammation,and then the cardiac hypertrophy and heart dysfunction.We can conclude that it may be the TNF-α that mediate the development of coronary heart disease（myocardial ischemia） syndromes.