C反应蛋白单体调控巨噬细胞表型漂移对心梗后心肌修复影响及机制

巨噬细胞主要分为M1和M2两个表型，M1型促进炎症反应，而M2型抑制炎症反应，促进修复。研究表明巨噬细胞由M1向M2型漂移对于心梗后心肌修复极为关键，因而明确调控心梗后巨噬细胞表型的因素将有助于损伤心肌的修复。我们的预实验结果首次发现C-反应蛋白单体（mCRP）出现于急性心肌梗死后，它参与了梗死后心肌损伤过程，导致梗死面积扩大，心功能恶化以及梗死区M1型巨噬细胞存在时间的延长。为此我们推测：mCRP可以通过调控巨噬细胞表型来影响心梗后炎症反应程度及持续时间，进而对心肌修复产生不良作用。为验证这一假说：本研究拟采用Western blot，qPCR及流式细胞术等手段在细胞和动物水平研究mCRP对巨噬细胞表型的影响；探讨该作用对心梗后心肌修复的影响。本研究将从mCRP对巨噬细胞表型影响与心肌修复方面阐述炎症与心梗关系，为急性心肌梗死的治疗提供新思路。

Macrophages can be classified as M1 and M2 subtypes, which are involved in the process of inflammation and repairment after acute myocardial infarction (AMI). The shift from M1 to M2 phenotye of macrophage plays a key role in myocardial repairment after AMI. Our previous results demonstrated that monomeric CRP (mCRP) is a potential new biomarker for AMI diagnosis. In addition, mCRP is involved in the process of cardiac damage after AMI, which can increase the myocardial infarction size and aggregate cardiac function deterioration. mCRP further can prolong the existing time of M1 macrophages in infarcted area. Accordingly, we then assume that: mCRP can aggrevate the damage of myocardial tissue via modulating the phenotype of macrophage after AMI. In our study, we will focus on the effects and the molecular mechanisms of mCRP on the phenotype of macrophages. We will further study the consequence of shifted phenotype of macrophages on myocardial repairment after AMI. This projects will provide new information for clarifying the relationship between inflammation and AMI, which will finally benefit the clinic treatment of AMI.