Study On Mechamism Of Astragalus Polysaccharides To Intervent AtheroSclerosis Of Vulnerable Plaques By Way Of"HSP60-TLR4/MyD88-Mmacrophages"

Objective:By observing the expression of Toll-like Receptor4(TLR4) and Myeloid differentiation primary response gene88(MyD88) in model of inflammatory cells and Interleukin-6(IL-6) and Tumor necrosis factor-a(TNF-a) in supernatant after intervention of astragalus polysaccharide(APS), to discuss its possible stability molecular mechanisms of vulnerable plaques in the heat shock protein60(HSP60) induced Macrophages (MO) activated immune inflammatory activaty.Method:Human acute monocyticleukemia cell strain (THP-1) was used as experimental object which was randomly divided into following four groups:the THP-1group, MΦ group, HSP60group and the APS group. For the first group, the THP-1was cultured for12hs, extracted the cell protein and collected the supernatant; Phorbol12-Myristatel3-Acetate(PMA) was used in the second group to induce the THP-1cells72hs to differentiate into MΦ, MΦ was cultivated subsequently for12hs, then extracted cell protein and collected supernatant; The third group used PMA to induce THP-1cells for72hs to differentiate into MO, the HSP60was used to subsequently culture cells for12hs then extracted cell protein and collected supernatant; The fourth group used PMA to induce THP-1cells for72h to differentiate into MΦ, then uses the APS to pretreatment for48h, subsequently use HSP60to culture cells for12h and extract cell protein and collect supernatant. The expression of related protein in cells and the concentrations of inflammatory factors in cell supernatant were detected by Western Blot and ELISA respectively.Results:1.Astragalus polysaccharide can significantly inhibit the expression of TLR4and MyD88protein in inflammatory MO;2. Astragalus polysaccharide can significantly low-regulate the concentration of IL-6and TNF-a in supernatant.Conclusion:Astragalus polysaccharide may exert stabling vulnerable plaques by inhabiting the activation of TLR4and MyD88proteins, low-regulating the inflammatory factors IL-6and TNF-a via "HSP60-TLR4/MyD88-MΦ".