Objective To investigate the effects of prenatal and postnatal exposure to bisphenol A on serum IL - 17 and IL - 23 of mouse offspring, and explore the mechanism of developmental immune toxicity of bisphenol A. Methods Confirmed pregnancy ICR mice were randomly divided into blank control, solvent control, 2. 0 g / L BPA ,0. 5 g / L BPA and 0. 125g/ L BPA groups. Gestation mice were exposed to BPA through drinking water from gestation day 0 ( GDO ) to offspring weaning ( postnatal days 21 , PND21 ). At PND7,PND21 and PND42, pups peripheral blood was taken and IL - 17 and IL -23 content in serum were assayed using ELISA. Results At PND7 and PND21 , IL - 17 and IL -23 content in serum of offspring increased gradually with exposure dose elevating in pregnancy mice, and the differences showed statistical significance between 2. 0 g / L BPA group and blank control group or solvent control group ( P < 0. 05 ). At PND42 , IL - 17 and IL -23 content in serum of offspring showed no significant difference between BPA exposed groups and blank control group or solvent control group ( P > 0.05 ). Conclusion Prenatal and postnatal BPA exposure may cause the increased cytokines secretion of Th17 cells before weaning in offspring.%目的 研究出生前后高剂量双酚A(BPA)暴露对小鼠不同时期血清白介素-17(IL-17)和白介素-23(IL-23)水平的影响,初步探讨BPA发育免疫毒性机制.方法 将确认妊娠的ICR母鼠随机分为空白对照组、溶剂对照组、BPA剂量组(高、中、低组分别为2.0、0.5和0.125 g/L BPA);母鼠自妊娠第0 d(GD0)至仔鼠断乳(出生后第21d,PND21)经饮水暴露于BPA.分别于PND7、PND21和PND42取仔鼠外周血用ELISA检测IL-17和IL-23含量.结果 在PND7和PND21时,随母鼠BPA暴露剂量的增加,仔鼠血清IL-17和IL-23含量逐渐上升,2.0 g/L BPA组与空白对照组和溶剂对照组相比,差异均有统计学意义(P值均<0.05).在PND42时,各BPA暴露组仔鼠血清IL-17和IL-23含量与空白对照组和溶剂对照组差异均无统计学意义(P值均>0.05).结论 出生前后BPA暴露可能引起子代断乳前体内Th17细胞分泌的细胞因子含量升高.
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