二恶英对子宫内膜异位症小鼠的免疫毒性

Immunotoxicity of TCDD on development of endometriosis in mouse model

目的探讨四氯二苯并二恶英(TCDD)对于子宫内膜异位症小鼠模型的免疫毒性。方法采用小鼠自体子宫内膜移植法建立小鼠子宫内膜异位症模型,间隔21d分别给予TCDD0、1、3、10μg/kg灌胃1次。建模术后3、6、9周处死,鉴定异位病灶的形成,测量异位病灶体积,摘取胸腺并称重,计算脏器系数。采用RT-PCR法检测各组小鼠异位子宫内膜组织中IL-1βmRNA水平。结果对照组异位子宫内膜病灶逐渐萎缩消失。随着染毒时间的延长和染毒剂量的增加,染毒组异位病灶体积明显呈剂量和时间依从性增加(P<0.05)。与对照组相比,染毒组胸腺脏器系数呈现时间和剂量依赖性降低(P<0.05)。异位灶体积和胸腺脏器系数之间具有明显的负相关性(P<0.05)。与对照组相比,染毒组小鼠异位子宫内膜中IL-1βmRNA表达较对照组明显呈剂量和时间依从性上调(P<0.01)。结论 TCDD可促进模型小鼠异位子宫内膜病灶的发展,其机制可能与系统性和局部性免疫毒性有关。

Objective To investigate the immunotoxicity effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin（TCDD） on development of endometriosis in a mouse model.Methods The endometriosis mouse model was established with autotransplantation of endometrium.Twenty-one days prior to induction surgery for endometriosis,female mice were pretreated with TCDD in a dose of 0,1,3 or 10 μg/kg.Animals were killed on the 3rd,6th or 9th week following surgery for measuring diameter of ectopic focuses,weighting the thymus gland and detecting IL-1β mRNA expression in ectopic focuses by RT-PCR assay.Results The ectopic focuses in the controlled mice were gradually atrophied and disappeared,which in TCDD-treated mice were enlarged in a time-and dose-dependent manner（P0.05）.Compared with control mice,the organ coefficient of the thymus gland in TCDD-treated mice showed a time-and dose-dependent decrease（P0.05）,which was negatively correlated with the mass of the thymus gland（P0.05）.Compared with control mice,IL-1β mRNA expression in TCDD-treated mice was up-regulated time-and dose-dependently（P0.01）.Conclusion TCDD can promote progression of ectopic focus of endometriosis in the mouse model,which may be related to its general and local immunotoxicity.