抄録
The cell models of SiO2 activating macrophages were set up in order to explore the roles of Annexin A5 in the activation. SiO2 produced an increase in the expression of Annexin A5, IL-1α and TGFβ1 in macrophages. When Annexin A5 knock-down by siRNA, the expression of IL-1α and TGFβ1 were decreased, and the secretive levels of TGFβ1 were also down-regulate. These foundings suggested that the expression of Annexin A5 activated macrophages and influenced the producing and relieving inflammatory cytokines and fibrotic factors. Recent years it was found that Fas-ligand cell signaling has a key role in the initial phase of lung fibrosis, so we studied on the protein expressions of Fas signal pathway. When SiO2 activited the macrophages, the expressions of Fas/FasL signal pathway molecules including FasL, were increased. However, when FasL knock-down by siRNA, the expression of IL-1α and TGFβ1 were decreased and the protein expressions in down stream, Fas, Casp8, Casp3, decreased, too, and the secretion of TGFβ1 from macrophages was also down-regulate. At last we explored the interaction between Annexin A5 and FasL in SiO2 activited macrophage models. It was found that Annexin A5 knock-down could decrease the expressiond of FasL, but Annexin A5 was up regulate when FasL knock-down. Those foundings suggested that Annexin A5 could effect on the activation of macrophage and has the interaction with Fas/FasL signal pathway.
