Tongmaiyizhi Capsule Apolipoprotein E Gene Knock On Impact, In Addition To The Mice Vulnerable Atherosclerotic Plaque Stability

BackgroudAtherosclerosis is by far the most frequent cause of ischemic disease,the plaque disruption with superimposed thrombosis is the main cause ofthe unstable angina, myocardial infarction, stroke and sudden death.Therefore, for event-free survival, the vital question is not whyatherosclerosis develops but rather why, after years of indolent growth,it suddenly becomes complicated by life-threatening thrombosis. So in nowdays how to stable the vulnerable atherosclerotic plaque become the mosturgent thing to deal with. Our experiment want to evaluate thehistomorphological change of the plaque to ensure wether the tongmaiyizhicapsule have the ability to stable the vulnerable plaque.Objective(1) find the system to evaluate the stability of vulnerableatherosclerotic plaque.(2) To investigate the effect of tongmaiyizhi capsule on advanced unstableatherosclerotic lesions within the innominate artery of ApoE-DeficientMice.MethodsThe 8week—old ApoE=Deficient Mice were randomly divided into threegroups:tongmaiyizhi group, model group and simvastatin group, six normalC57BL/6 mice were set as the control group, all the mice were fed withhigh fat diet for 22 weeks and then tongmaiyizhicapsule (720mg/Kg/d) andsimvastatin (2.8mg/Kg/d) was administered to 30week—old Apoe—DeficientMice for 8 weeks in simvastatin and tongmaiyizhi group and the other modelgroup were administered with Sodium Chloride. The immunochemistry,Movat pentachrome and Sirius red—victoria blue staining methods wereused to evaluate the histomorphological change of the plaque. ResultsContrast with model group: The average area of AS lesion decreased andthe content of collagen were significantly increased (P＜0.01, P＜0.05)in tongmaiyizhi capsule group; The thickness, integrity of the fibrouscap were all better than the controls in simvastatin group (P＜0.05, P＜0.05); but the two drugs have no use to decrease the incidence rateof calcification, the large necrotic core and the disrupt internal elasticlamina and the thrombosis.ConclusionsOur experiments shows that the two drugs have the ability to stabilizethe vulnerable atherosclerotic plaque.