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目的:观察黄芪多糖对“轻度氧化修饰低密度脂蛋白(mm LDL)-Toll样受体4(TLR4)-巨噬细胞”途径的干预作用,探讨其稳定动脉粥样硬化(AS)斑块、抑制AS进展的分子机制。方法:将THP-1源性巨噬细胞分为空白组,模型组,黄芪多糖低、中、高剂量。采用免疫印迹法检测脾酪氨酸激酶(Syk)、细胞外信号调节激酶(Erk)、桩蛋白(Paxillin)磷酸化水平随时间变化情况,以及不同剂量黄芪多糖对Syk、Erk、Paxillin蛋白磷酸化水平的影响;采用免疫沉淀联合免疫印迹法检测TLR4蛋白磷酸化水平随时间变化情况,以及不同剂量黄芪多糖对TLR4蛋白磷酸化水平的影响;采用中性红吞噬实验检测黄芪多糖对巨噬细胞吞噬功能的影响。结果:TLR4、Syk、Erk、Paxillin分别于15、10、15、30min达到磷酸化水平高峰;与空白组比较,模型组TLR4、Syk、Erk、Paxillin磷酸化水平升高(P<0.05)、细胞吞噬功能增强(P<0.05);与模型组比较,黄芪多糖低、中、高剂量组TLR4、Syk、ERK、Paxillin磷酸化水平降低(P<0.05)、细胞吞噬功能减弱(P<0.05);其中,黄芪多糖高剂量组上述改变明显强于黄芪多糖低、中剂量组(P<0.05)。结论:黄芪多糖可能通过“mm LDL-TLR4-巨噬细胞”途径影响巨噬细胞吞噬功能从而具有稳定AS斑块、干预AS作用。
OBJECTIVE: To observe the effect of astragalus polysaccharides on the “mild LDL-TLR4-macrophage” pathway and to explore its role in the pathogenesis of stable atherosclerosis (AS) Plaque, the molecular mechanism of inhibiting the progression of AS. Methods: The THP-1-derived macrophages were divided into blank group, model group, Astragalus polysaccharide low, medium and high dose. Western blotting was used to detect the changes of phosphorylation of Syk, Erk and Paxillin, and phosphorylation of Syk, Erk and Paxillin by different doses of Astragalus polysaccharides The effect of astragalus polysaccharide on TLR4 protein phosphorylation was examined by immunoprecipitation and Western blotting. The effect of APS on macrophage phagocytosis Effect of function. Results: The phosphorylation levels of TLR4, Syk, Erk and Paxillin reached the peak at 15, 10, 15 and 30 minutes respectively. Compared with the blank group, the phosphorylation levels of TLR4, Syk, Erk and Paxillin in the model group increased (P < (P <0.05). Compared with the model group, the phosphorylation of TLR4, Syk, ERK and Paxillin of astragalus polysaccharide group decreased (P <0.05) and the phagocytic function of astragalus polysaccharide group decreased (P <0.05). Among them, the high-dose group of Astragalus polysaccharide was significantly higher than the low-dose and medium-dose groups (P <0.05). Conclusion: Astragalus polysaccharides may affect the phagocytosis of macrophages through the “mm LDL-TLR4-macrophage” pathway to stabilize AS plaques and interfere with AS.