Objective To study the impact of acrylonitrile(AN)on Bcl10 protein and mitogen activated protein kinase in signal transmission and to explore the mechanism of its immune-toxicity in rat.Methods Jurkat cell lines were divided into control group and three AN exposed groups,i.e.low concentration group(20 umol/L),medium concentration group(100 umol/L)and high concentration group(500 umol/L),and cultivated in vitro.Lipid raft and Bc110 protein were separated and analyzed.Levels of MEK1 and p-MEK1 were detected by Western Blot.Results As AN concentration of exposure increased,the total amount of Bcl10 kept unchanged;however,the location concentrated mainly in lower area.Western Blot results showed that in a definite range of exposure the secretion of MEK1 protein increased.After the exposure exceeded the definite concentration,the secretion of MEK1 protein decreased,and the concentration of P-MEK1 increased as the exposure increased showing a tendency of gradual lowering.In comparison with the control,the difference showed statistical significant(P0.05).Conclusions AN may produce the immune toxicity through damaging the lipid raft structure and causing the separation of Bcl10 protein and lipid raft,finally inhibiting the mitogen activated tyrosine kinase signal transmission pathway.

采取体外细胞培养技术,将T淋巴细胞Jurkat细胞株分为空白对照组和丙烯腈(acrylonitrile,AN)低浓度、中浓度、高浓度染毒组,AN浓度分别为20、100、500μmol/L。采用蔗糖密度梯度低温超速离心技术对细胞膜脂筏进行分离,利用FACS技术结合β-环湖精去除脂筏内胆固醇,并对脂筏内信号蛋白分子Bcl10进行分析。结果显示,随染毒浓度增加,各染毒组细胞膜胆固醇含量下降,与对照组相比,差异有统计学意义(P<0.05),提示脂筏数量越少。Bcl10蛋白偏离脂筏正常情况下应该所在的密度层面。