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目的:探究Src对动脉粥样硬化斑块中巨噬细胞脂质累积的调控机制。方法:取发生动脉粥样硬化的股动脉(病变组)与正常乳内动脉(对照组)组织,免疫组织化学法检测组织中磷酸化Src表达水平。采用Src干扰小RNA(siRNA)转染和Src蛋白激酶特异性抑制剂PP2处理巨噬细胞,通过油红O染色及比色法测定其胞内脂质含量,探究Src对巨噬细胞脂质累积的作用机制。通过构建C57BL/6小鼠动脉粥样硬化模型,进一步确定Src在动脉粥样硬化过程中的重要作用。结果:与正常对照相比较,动脉粥样硬化斑块中磷酸化Src表达量明显升高(P<0.05),且与CD68阳性细胞(巨噬细胞)共定位良好;降低Src表达水平和活性后,氧化低密度脂蛋白(oxLDL)诱导的巨噬细胞内脂质累积减少(P<0.05)。结论:Src可能通过介导巨噬细胞脂质累积调控动脉粥样硬化斑块的形成。
OBJECTIVE: To investigate the regulatory mechanism of Src on macrophage lipid accumulation in atherosclerotic plaque. Methods: Tissue samples of atherosclerotic femoral artery (diseased group) and normal internal mammary artery (control group) were collected. The phosphorylated Src expression was detected by immunohistochemistry. Macrophages were treated with Src-siRNA and Src kinase inhibitor PP2, and their intracellular lipid contents were determined by oil red O staining and colorimetric assay. The effects of Src on macrophage lipid accumulation The mechanism of action. Through the construction of C57BL / 6 mouse atherosclerosis model, to further determine the important role of Src in the process of atherosclerosis. Results: Compared with the normal controls, the expression of phosphorylated Src in atherosclerotic plaques was significantly increased (P <0.05), and co-localized with CD68 positive cells (macrophages). The Src expression level and activity were decreased , While the lipid accumulation in macrophages induced by oxLDL decreased (P <0.05). Conclusion: Src may regulate the formation of atherosclerotic plaque by mediating the accumulation of macrophages lipid.