| Background and aimThe important role of inflammation in CHD is recognized gradually, during this process of inflammation, with the interaction of endothelial cell, leucocyte and blood platelet as well as endothelium, leucocyte emgriated through endothelial cells, which led to inflammatory reaction and thrombosis, accelerating the formation and development of CHD. As we know, during this process, cell adhesion molecules are the basic factor. Thus, the study of CAM will develop a new prospect to diagnosis, treatment and prevention to CHD. In our study, we observed the effect of QDTMT on expression of ICAM-1 in vitro myocardial cell and ICAM-1 and P-selectin in vivo of myocardial ischemic rats. The purpose ofthis study is to supply reliable experimental basis for the clinic application of this medicine.Methods1. Cultured rat myocardial cells stimulated with TNF-a at the indicated concentration (100U ml-1) for various time (6, 12, 24h), at the same time, we treated the cells with QDTMT, cell surface expression of ICAM-1 was detected by immunocytochemistry methods.2. The aim of Experiment II is to investigate the role of QDTMT on injury myocardium by Iso: Rats were randomly divided into four groups (control, model, QDTMTmax, QDTMTmin) and gastrogavaged with either saline or extract of QDTMT (1g.kg-1) and QDTMT (2g.kg-1) respectively for 14 days, then given celiac injection of isoproterenol (4mg.kg d-1) and the ischemic model was established, then removing the rat heart, making myocardium section preparation. We detected expression of ICAM-1 and P-selectin in the ischemic myocardium by immunohistochemistry.3. The aim of Experiment III is to investigate the role of QDTMT on injury myocardium of acute myocardial ischemia: Rats were randomly divided into four groups (control, model, QDTMTmax, QDTMTmin) and gastrogavaged with either saline or extract of QDTMT (Ig.kg-1) and QDTMT (2g.kg-1) respectively for 14 days, then duplicating rabbit model of acute myocardial ischemia by means of ligating left anterior descending branch of coronary artery, observing and measuring dynamic characteristics of cardiac mechanical function, indexes such as PEP, LVET, P/L, ICT, I/L are included, then removing the rat heart, making myocardium section preparation, the ICAM-1 and P-selectin expression in the ischemic myocardium were observed by immunohistochemistry.Results1. TNF-a can stimulate expression of ICAM-1 on myocardium remarkably, especially in 12h and with the time on it decreased, but QDTMT can reducecell surface expression of ICAM-1 significantly (P<0.05 or 0.01) on every time.2. Expression of ICAM-1 and P-selectin in group of control are mostly negative, but in Model most are positive on impaired myocardium by isoproterenol (ICAM-1 85 % , P-selectin 78 %), after treated with QDTMT we can see that positive expression decreased significantly (P<0.01).3. Expression of ICAM-1 and P-selectin on acute impaired myocardium increased, but we found that QDTMT was remarkably reduced expression of ICAM-1. Also we can find treated with QDTMT, area of myocardial infarction decreased significiently, which is as the same as previous study. After ligating left anterior descending branch of coronary artery, we found that QDTMT high and low dose can reduce prolonged PEP, ICT after ischemia, decrease the elevatory P/L and I/L, enchance LVET.Conclutions1. QDTMT can remarkably reduced expression of ICAM-1 in cultured rat myocardial cells stimulated with TNF-a.2. QDTMT can protect impaired myocardium by Iso through reducing the expression of ICAM-1 and P-selectin.3. QDTMT can protect acute impaired myocardium by reducing the expression of ICAM-1 and P-selectin. QDTMT can protect impaired myocardium by ligating left anterior descending branch of coronary artery through decreasing area of myocardial infarction, improving the systolic function of injury myocardium, probably this role of QDTMT is related to its effect on the exp...
|
PDF Full Text Request