冠心康含药血清通过活化ERK5对ox-LDL负载的巨噬细胞胞葬作用的影响(英文)

发布时间：2024-02-04 17:23

　　目的:探讨冠心康通过活化ERK5抗动脉粥样硬化的潜在分子机制.方法:用ERK5抑制剂(ERK5-IN-1和XMD8-92)干预RAW264.7细胞,探讨ERK5失活对巨噬细胞胞葬作用的影响.用ox-LDL干预RAW264.7细胞建立巨噬细胞胞葬作用功能受损的细胞模型,然后在存在或不存在XMD8-92干预的情况下,用冠心康含药血清处理该细胞模型.流式细胞仪检测巨噬细胞的胞葬率,RT-qPCR和Western blot法检测巨噬细胞ERK5和C1qA的mRNA和蛋白的表达.结果:ERK5抑制剂XMD8-92和ERK5-IN-1均可抑制RAW264.7细胞的胞葬作用,抑制ERK5的活化和C1q A mRNA和蛋白的表达.冠心康含药血清可增强ox-LDL导致的受损的巨噬细胞胞葬作用,这一作用与冠心康活化ERK5和上调C1q A mRNA和蛋白的表达有关.结论:ERK5激酶的失活可通过下调C1qA的表达损伤巨噬细胞胞葬作用;冠心康可通过活化ERK5上调C1qA的表达,促进ox-LDL负载的巨噬细胞胞葬作用.

【文章页数】：14 页

【文章目录】：
1 Materials and methods
    1.1 Materials
        1.1.1 Animals and cells
        1.1.2 Reagents and drugs instruments
    1.2 Experimental design
        1.2.1 Preparation of GXK decoctions and rat medicine serum
        1.2.2 Treatment of RAW264.7 cells
        1.2.3 Effect of ERK5 inhibitors on RAW264.7 cells
        1.2.4 Complement component C1q effect of ox-LDL on RAW264.7 macrophage efferocytosis
        1.2.5 Effect of medicated serum on ox-LDL-loaded macrophages
    1.3 Experimental methods
        1.3.1 Efferocytosis assay
        1.3.2 RT-qPCR
        1.3.3 Western Blot analysis
    1.4 Statistical analysis
2 Results
    2.1 ERK5 inhibitors suppressed macrophage efferocytosis in vitro
    2.2 ERK5 inhibitors suppressed ERK5 activation and expression of C1qA in macrophages
    2.3 Ox-LDL weakened macrophage efferocytosis
    2.4 GXK improved efferocytosis of ox-LDL-loaded macrophages by activating ERK5
    2.5 GXK upregulated C1qA expression via ERK5 activation in ox-LDL-loaded macrophages
3 Discussion
4 Conclusion



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