在动脉粥样硬化（atherosclerosis，AS）进展期，坏死核形成、斑块破裂常易引发急性心脑血管事件的发生。巨噬细胞介导的胞葬作用被认为可以限制AS的进展，ERK5及其相关信号通路在巨噬细胞胞葬过程中至关重要，但这一过程的具体机制尚未明了。.本研究拟通过体内外实验，建立ERK5-MKO/LDLR-/-动脉粥样硬化小鼠及巨噬细胞模型，采用分子生物学技术，观察AS发展过程中巨噬细胞吞噬指数，ERK5及其下游转导通路、胞葬作用相关的识别与非识别、吞噬与非吞噬信号基因和蛋白的表达以及斑块成分的变化，并观察具有益气活血、化痰降浊之功效的中药复方冠心康及其拆方的干预作用，明确冠心康及其拆方延缓进展期AS易损斑块和坏死核形成的分子机制。

The formation of necrotic cores and and disruption of vulnerable plaques in advanced lesion of atheroclerosis(AS) often cause the occurrence of acute cardiocerebro-vascular events.Efferocytosis of macrophage is able to control the progress of atherosclerosis,ERK5 and its related signaling pathway play an important role,but its mechanism is unknown..This research designed to establish rats and macrophages AS model of ERK5-MKO/LDLR-/- in vivo and in vitro, by the use of molecular biology techniques,to observe the phagocytic index of the macrophages, ERK5 and its downstream pathway, genes and proteins of "find-me","not find-me","eat-me","not eat-me" signals related to the efferocytosis,the composition of plaque. And observe the intervension of Guanxinkang prescription and its composition,which can supplement qi,activate blood circulation and remove phlegm evil,so that to provide the molecular mechanism of Guanxinkang prescription and its composition on the delay of the formation of vulnerable plaques and necrotic cores in advanced AS.