摘要
目的探讨二噁英致子宫内膜异位症发病可能的作用机制。方法（1）60只小鼠建立子宫内膜异位症模型，分别给予二噁英（TCDD）灌胃染毒，每21天1次，于建模术后3、6、9周处死，鉴定异位病灶的形成，测量异位病灶面积；②按处死时间随机分为3周组、6周组、9周组，每组20只；每组再随机分成4个剂量组，分别是：对照组（给玉米油）、低剂量染毒组（1μg／kgTCDD）、中剂量染毒组（3μg／kgTCDD）和高剂量染毒组（10μg／kgTCDD）；③采用半定量逆转录一聚合酶链反应检测不同染毒剂量组小鼠模型子宫内膜异位症异位病灶中白细胞介素-1β（IL-1β）mRNA的表达水平。结果①随TCDD染毒时间的延长和染毒剂量的增加，小鼠子宫内膜异位病灶面积相应增加，F值分别为107．349和171．408，均P〈0．05；②小鼠子宫内膜异位病灶中白细胞介素-1βmRNA表达的上调，随TCDD染毒时间延长，值分别为10．600、10．656和12．182，均P〈0．05；随染毒剂量的增加，中剂量组和高剂量组F值分别为10．332和11．347，均P〈0．05）。结论TCDD染毒促进了小鼠子宫内膜异位症模型异位病灶的发展，白细胞介素-1β表达上调可能是TCDD促异位病灶发展的作用机制之一。
Objective To investgate possible mechanism that dioxin induces development of endometriosis （EMs）. Methods （1）60 ICR mice were expoured to 0, 1,3 or 10μg/kg of 2,3,7,82tetrachlorodibenzo,p-dioxin（TCDD） once per 21 days with administration by gavage respectively to establish a mouse EMs model . The mice were killed at the 3th, the 6th and the 9th weeks after establishment of the model and ectopic focus of EMs formed in mice body was indentified and area of the ectopic focus was measured; （1）The mice were individed into three groups according to killing time of the mice： 3-week group, 6-week group and 9-week group （in each group n = 20） and the mice in each group were further divided into four subgroups randomly： control group （the mice were given corn oil）, low dose of TCDD exposure subgroup （ the mice were given 1μg/kg of TCDD）, middle dose of TCDD exposure subgroup （ the mice were given 3μg/kg of TCDD ） and high dose of TCDD exposure subgroup （the mice were given 10μg/kg of TCDD） ; （3）The expression of IL-1β in the ectopic focus of EMs model of mice in different doses of TCDD exposure groups was determined by semi-quantitative RT-PCR. Results （1）With prolongation of TCDD expostre：and increase in TCDD dosage, the area of the ectopic focus of EMs was increased correspondingly （F = 107. 349, 171. 408 respectively, both P〈0.05） ; （2）With prolongation of TCDD exposure （F= 10. 600, 10. 656, 12. 182 respectively, all P 〈0.05） and increase in TCDD dosage （for the middle and high doses of TCDD exposure subgroups： F = 10. 332, 11. 347 respectively, both P 〈 0.05）, the expression of IL-1β mRNA in the ectopic focus tissues was up-regulated compared with the control group. Conclusion Environmental dioxins （TCDD） may promote growth of ectopic focus in a mouse model of EMs, and up-regulation of expression of IL-1β may be one of mechanisms that TCDD promotes growth of the ectopic focus of EMs.
出处
《中国妇幼健康研究》
2011年第2期162-164,共3页
Chinese Journal of Woman and Child Health Research
