S100-B通过p38MAPK促进Jurkat细胞表达IFN-γ

S100-B induce expression of IFN-γ via p38MAPK in Jurkat cells

目的:探讨S100-B对Jurkat细胞核分泌炎症因子Interferon-γ(IFN-γ)的影响及相关信号分子改变。方法:S100-B作用于植物血凝集素(PHA)预刺激的Jurkat细胞,Western blot检测S100-B诱导Jurkat细胞NF-κB与p38MAPK磷酸化水平的变化;ELISA检测S100-B诱导Jurkat细胞分泌IFN-γ。结果:S100-B作用24 h后,Jurkat细胞表达NF-κB增多,上清中检测到IFN-γ达201 pg/ml,明显高于阴性对照组(123 pg/ml)。S100-B可引起p38MAPK磷酸化,p38MAPK阻滞剂明显抑制S100-B诱导的IFN-γ表达。结论:S100-B促进PHA预刺激的Jurkat细胞表达NF-κB,促进Jurkat细胞分泌IFN-γ,其机制与激活p38MAPK途径有关。

Objective：To investigate the role of S100-B on the expression of IFN-γ and associated signaling pathway in Jurkat cells. Methods： The expression of NF-KB was assessed by Western blot and the secretion of IFN-γ was tested by ELISA. In addition, total and phosphorylated p38MAPK was measured by Western blot,too. Results： S100-B enhanced the expression of NF-KB in Jurkat cells,Sl00-B induced Jurkat cells expressing IFN-γ,promoted p38MAPK phosphorylate. And, p38MAPK inhibitor inhibited S100-B-in- duced IFN-γ expression. Conclusion： S100-B promotes IFN-γ expression via p38MAPK in Jurkat ceils which pre-stimulated by phyto- hemagglutinin （PHA）.