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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 toxic effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the secretion of antibody against B lymphocyte strain CH12.LX and its possible receptor mechanism. Methods The B lymphocyte strain CH12.LX was used as a cell model. The effects of serial concentrations of TCDD treatment on IgM secretion by LPS-activated CH12.LX were detected by ELISA. The aromatics of CH12.LX cells were detected by RT-PCR and Western blot Receptor (AhR) expression level, as well as TCDD on cytochrome P450Cyp1a1 induction effect. Results TCDD (0.03 nmol / L) significantly inhibited IgM secretion of CH12.LX (P <0.05), while TCDD (10 nmol / L) significantly induced CH12.LX intracellular Cyp1a1 mRNA expression (P <0.05), and found that there was a certain level of expression of AhR in CH12.LX cells. Conclusion TCDD has significant inhibitory effect on the secretion of CH12.LX from B lymphocyte strain. At the same time, it is speculated that this immunotoxic effect of TCDD may be mainly mediated by AhR.