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目的:观察炎症因素诱导大鼠动脉粥样硬化发病过程中对血管内皮细胞的影响。方法:实验分为单纯高脂对照组和炎症组,分别腹腔注射给予无菌医用液体石蜡和酵母多糖(Zym,20mg/kg,1次/3天)。所有大鼠均喂食含3%胆固醇的高脂饲料,共8周。透射电镜观察主动脉超微结构;应用定量PCR法测定腹主动脉组织中诱导型一氧化氮合酶(iNOS)mRNA、血管细胞粘附分子(VCAM)-1 mRNA、以及基质金属蛋白酶7(MMP7)mRNA的表达。结果:炎症组可见游走于内膜下层的平滑肌细胞和和吞噬脂质颗粒的单核细胞,单纯高脂对照组仅见内皮细胞损伤和退行性变,未见内膜下层形成泡沫细胞,AS样病变较炎症组轻。与对照组相比,炎症组动脉壁iNOS mRNA表达降低,VCAM-1 mRNA及MMP7 mRNA标大量显著升高。结论:炎症刺激能够损伤动脉血管内皮细胞,诱导炎症因子释放增加,促进动脉粥样硬化的发生。
Objective: To observe the effect of inflammation on vascular endothelial cells in the pathogenesis of atherosclerosis in rats. Methods: The experiment was divided into simple hyperlipidemic control group and inflammatory group. Sterile medical liquid paraffin and zymosan (Zym, 20mg / kg, once / 3 days) were injected intraperitoneally. All rats were fed a high-fat diet containing 3% cholesterol for 8 weeks. The ultrastructure of the aorta was observed by transmission electron microscopy. The expressions of iNOS mRNA, VCAM-1 mRNA and MMP-7 mRNA in abdominal aorta tissue were detected by quantitative PCR. ) mRNA expression. Results: In the inflammatory group, smooth muscle cells and monocytes phagocytosed with lipid particles were observed in the subendothelium. Only the hyperlipidemic control group showed endothelial cell injury and degenerative changes only. No foam cells formed in the subendothelium. AS-like Lesions than inflammation group light. Compared with the control group, the expression of iNOS mRNA in the arterial wall of inflammatory group decreased significantly, and the mRNA of VCAM-1 mRNA and MMP7 significantly increased. Conclusion: Inflammatory stimuli can damage arterial endothelial cells, induce the release of inflammatory cytokines and promote the development of atherosclerosis.