单核巨噬细胞偏极分化在斑块炎症形成中的作用内科学(心血管病学)专业论文.docx

单核巨噬细胞偏极分化在斑块炎症形成中的作用内科学(心血管病学)专业论文.docx

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单核巨噬细胞偏极分化在斑块炎症形成中的作用内科学(心血管病学)专业论文

汕头 汕头大学医学院硕士学位论文 汕头 汕头大学医学院硕士学位论文 PAGE PAGE III PAGE PAGE IV Abstract Background: Monocyte/macrophage line plays vital role in the formation of atherosclerotic inflammation. However, the role of monocyte/macrophage subline is ill defined. Monocyte differentiate into two major macrophage phenotypes in subendothelial layer, the classic pro-inflammatory M1 and alternative anti-inflammatory M2 phenotypes, they are regulated by signals from the surrounding milieus. Each phenotype discloses different features in the role of inflammation. M1 macrophage highly express pro-inflammatory molecules, serve novel pro-inflammatory role. Partial M1 polarization result in uncontrolled inflammatory pathogenesis. While anti-inflammatory repair M2 macrophage highly expresses IL-10, IL-4, CD163 and HO-1, serve a vital role in effective efferocytosis, anti- inflammatory and anti-oxidation. Peripheral monocytes were well classified three major phenotypes: “classical” mon1, “intermediate”, mon2 and “non-classical” mon3. They are heterogeneous groups feature with different differentiate potential and distinct expression of cell-surface markers, chemokine receptors, and functions during inflammatory responses. Aim: To identified the role of monocyte/macrophage subset in CAD patients and different coronary qlaques, to illustrate their role in the formation of atherosclerotic inflammation. Methods: Enrolled patients were divided into 4 groups. 18 chest oppression (CHO, whose coronary angiogram is normal), 14 stable angina pectoris (SAP), 15 unstable angina pectoris (UAP) and 16 acute myocardial infarction (AMI). (1). CD14+CD163++ was used as mon2 biomarker. The CD14++CD163++monocyte proportions, CD163 mean fluorescence intensity (MFI) and CCR2 MFI were evaluated in these 63 patients. (2). Immunofluorescence staining of CD163, HO-1 was also study in 3 normal coronary arteries, 9 fibrous plaques and 5 advanced plaque to identify M2 macrophage subline in the plaque. Result: (1). Mon2 prop

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