【摘要】 目的:探讨力学拉伸对巨噬细胞极化的影响及可能涉及的机制。方法:对Raw264. 7细胞施加5%幅度力学拉伸,活/死细胞染色检测拉伸对细胞生长的影响;运用流式细胞仪及RT-PCR检测拉伸对细胞表面标志物及相关基因表达量的影响;Western blot检测NF-κB信号通路中蛋白表达量的影响。结果:5%幅度的细胞拉伸并不会对Raw264. 7细胞的生长造成影响,但Raw264. 7细胞表面M1极化分子CD86的表达显著减少,M2极化分子CD206的表达显著增加,CD86/CD206的比例下降;同时抗炎细胞因子基因的表达明显上调。此外,5%幅度拉伸降低了NF-κB信号通路中NIK和Pi-P65蛋白的表达量。结论:5%幅度的细胞拉伸抑制了NF-κB信号通路的激活从而促进Raw264. 7细胞向M2方向极化。更多还原

【Abstract】 Objective: To investigate the effect and mechanism of cyclic tensile strain on the polarization of macrophages. Methods: The effect of 5% cyclic tensile strain on cell growth was detected by live/dead cell staining. Flow cytometry and RT-PCR were used to detect the effect of cyclic tensile strain on cell surface markers and gene expression. To explore the effect of protein expression on NF-κB signaling pathway through Western blot. Results: 5% cyclic tensile strain had no effect on the cell growth,while,the expression of CD86 protein on Raw264.7 surface significantly reduced and CD206 protein increased;at the same time,5% cyclic tensile strain reduced the expression of inflammatory genes and increased the expression of anti-inflammatory genes significantly;5% cyclic tensile strain effectively inhibited the expression of NIK and Pi-P65 protein. Conclusion: 5% cyclic tensile strain can inhibit the polarization of Raw264.7 cells to M1 macrophage and promote the polarization toward M2 macrophage by inhibiting the activation of NF-κB signaling pathway.更多还原