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目的丙烯腈染毒T淋巴细胞,分析膜脂筏及Ras/Raf/MEK/ERK信号通路中MEK蛋白变化,探讨丙烯腈免疫毒性的可能作用机制。方法采取体外细胞培养技术,以T淋巴细胞Jurkat细胞株为研究对象,分为空白对照组、低浓度、中浓度、高浓度丙烯腈(0、20、100和500μmol/l)细胞染毒组,分析膜脂筏Caveolin-l蛋白、MEK蛋白变化。结果随染毒浓度增加,受检细胞经处理4 h后各染毒组与对照组细胞膜胆固醇含量差异有统计学意义(P<0.05),细胞膜胆固醇的含量下降,间接表明脂筏的数量越少;Caveolin-l蛋白定位改变,变构便于信号传递;p-MEK蛋白随浓度增高条带变浅。结论丙烯腈可能通过破坏脂筏结构,脂筏数量减少,Caveolin-l蛋白位移变构,Ras/Raf/MEK/ERK信号传导过程受到抑制而发挥免疫毒性。
Objective To investigate the changes of MEK protein in membrane lipid rafts and Ras / Raf / MEK / ERK signaling pathway by acrylonitrile-exposed T lymphocytes and to explore the possible mechanism of acrylonitrile immunotoxicity. Methods The in vitro cell culture technique was used to investigate the effects of different doses of Jurkat on T lymphocyte cell line Jurkat. The cells were divided into blank control group, low, medium and high concentrations of acrylonitrile (0, 20, 100 and 500 μmol / l) Analysis of membrane lipid raft Caveolin-l protein, MEK protein changes. Results With the increase of exposure concentration, the content of cholesterol in cell membrane decreased significantly after exposure for 4 h to the control group (P <0.05), which indirectly indicated that the number of lipid rafts ; Caveolin-l protein localization change, allosteric facilitate signal transmission; p-MEK protein with increasing concentration of the band becomes shallow. Conclusion Acrylonitrile may exert its immunotoxicity by inhibiting the structure of lipid raft, reducing the number of lipid rafts, and displacing the expression of Caveolin-1 protein and inhibiting the signal transduction of Ras / Raf / MEK / ERK.