| ObjectiveAcute myocardial infarction(AMI) is a major type of coronary heart disease, and many inflammatory cytokines are released at the area of infarction and its near areas after AMI, which have impacts on path physiology and prognosis of AMI. Recent researches have indicated emodin can adjust the release of inflammatory cytokines and has a protective effect on myocardial cells. But the report on how emodin affects the release of inflammatorycytokines has not appeared yet. Through ligating the left anterior descending coronary artery(LAD) to build the model of AMI, and using to remedy AMI, the experimental research will observe the therapeutic effects of emodin and preliminarily study its mechanism from the aspect of activative inflammatory cytokines.MethodsMale mice five weeks old from Kunming family were divided into five groups at random;①Sharm group;②Model group;③Contrast group;④high dosage group of emodin(H group);⑤low dosage group of emodin(L group). The mice were anaesthetized by 20% urethane, then intubated through oral tracheal and performed left anterior thoracotomy between the region of fourth and fifth intercostals, finally ligated the left anterior descending coronary artery(LAD) (LADs of the mice of Sharm group were not ligated). Accept Sharm group and Model group were not injected, other three groups were injected drugs into the abdominal cavities from the first day after the operation. Contrast group was injected 0.4ml admixture of DSMO and Tueen-80 each day during two weeks. H group and L group were separately injected 0.4ml and 0.2ml emodin liquid which density was 200ug/ml each day during two weeks. After two weeks, observe the effects of emodin on myocardial pathologic section, the heart function, the area of infarction, the density of TNF-α,IL-6 and the expression of MCP-1 in myocardial tissue.Results1. In myocardial pathologic changes, endocardial tissue was intact myocardial cells were normal in Sharm group. Endocardial tissue presented a big piece of necrosis and infiltration of many inflammatories in Model group, Endocardial tissue presented a small piece of necrosis and infiltration of a few inflammatories in H group, Endocardial tissue presented a relatively big piece of necrosis and infiltration of inflammatories in L group.2. Compared with Sharm group, LVSP and±dp/dtmax were obviously decreased, and LVEDP, the density of TNF-αand IL-6, the expression of MCP-1 in myocardial tissue were obviously increased in Model group(P＞0.05).3. Compared with Model group, all theLVSP,±dp/dtmax, LVEDP, the area of infarction, the density of TNF-αand IL-6, the expression of MCP-1 in myocardial tissue were not obviously different in Contrast group(P＞0.05).4. Compared with Model group and Contrast group, LVSP and±dp/dtmax was obviously inhanced, and LVEDP, the area of infarction, the density of TNF-αand IL-6, the expression of MCP-1 in myocardial tissue were obviously decreased in both H group and L group(P＜0.05).5. Compared with L group, LVSP and±dp/dtmax were obviously enhanced, and LVEDP,the area of infarction, the density of TNF-αand IL-6,the expression of MCP-1 in myocardial tissue was obviously decreased in H group(P＜0.05).Conclusion1. The animal models of AMI were obtained by thorax operation and ligating the left anterior descending coronary artery of mice. This provided the practical disease model to study mechanisms and prevention for AMI.2. Emodin has protection for AMI by improving the heart function and decreasing the area of infarction.3. Emodin can decrease the density of TNF-αandIL-6, the expression of MCP-1 in myocardial tissue. This effect is perhaps one of important mechanisms for protecting AMI. |
