摘要
目的探讨2,3,7,8-四氯二苯-对-二噁英(TCDD)对B淋巴细胞株CH12.LX的抗体分泌功能的毒性效应,及其可能的受体机制。方法以B淋巴细胞株CH12.LX为细胞模型,以ELISA法检测系列浓度TCDD处理对LPS活化CH12.LX的IgM分泌功能的影响,以RT-PCR和Western blot法检测CH12.LX细胞内芳香烃受体(AhR)的表达水平,以及TCDD对细胞色素P450Cyp1a1的诱导效应。结果较低浓度的TCDD(0.03nmol/L)即对CH12.LX的IgM分泌能力产生了显著的抑制效应(P<0·05),同时TCDD(10nmol/L)可显著诱导CH12.LX细胞内Cyp1a1 mRNA的表达(P<0·05),并于CH12.LX细胞内发现AhR有一定水平的表达。结论TCDD对B淋巴细胞株CH12.LX存在显著的抗体分泌抑制效应;同时,推测TCDD的这一免疫毒性效应主要可能由AhR介导。
Objective To investigate the possible toxic effects of TCDD on IgM secretion of LPS activated CH12. LX ceils, and its receptor mechanism. Methods The IgM level of LPS activated CH12. LX was measured with ELISA after treatment of serial concentrations of TCDD. AhR mRNA and protein expression level in CH12. LX was determined with RT-PCR and Western blot. The TCDD-induced expression of Cyplal mRNA was quantitated with real-time PCR analysis. Results The IgM secretion of LPS activated CH12. LX was significantly suppressed by TCDD ( ≥0.03 nmol/L) treatment (P 〈0. 05). Then TCDD induced Cyplal mRNA expression was also observed (P 〈 0. 05 ). AhR mRNA and protein expression was assured at a considerable level in CH12. LX ceils. Conclusion TCDD has a significant immunosuppression effect on CH12. LX cells. This effect is hypothesized to be mediated through AhR signal pathway.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2007年第12期1200-1202,共3页
Journal of Third Military Medical University
基金
第三军医大学科研基金(XG200550
XG200554)
总后"115"国际合作项目(06H024
06H028)~~