摘要
目的研究碘过量对环孢霉素A(Cyclosporin A,CsA)抑制实验性自身免疫性甲状腺炎(EAT)形成的拮抗作用,进一步探讨碘在自身免疫性甲状腺炎发病中的作用。方法给予Lewis大鼠不同碘摄入量,EAT诱发组和EAT+CsA组均用猪Tg进行免疫诱发EAT形成,EAT+CsA组于首次免疫后的第10 d开始腹腔注射CsA,5 mg/(kg.d),非EAT对照组不做任何处理,末次免疫后2周处死各组大鼠并取材。观察大鼠甲状腺组织的病理改变和炎细胞浸润程度,采用放射免疫法检测血清中甲状腺球蛋白抗体(TG-Ab)、甲状腺过氧化物酶抗体(TPO-Ab)和T3、T4水平。结果(1)不同碘摄入量的EAT组和EAT+CsA组的大鼠甲状腺组织均有不同程度的炎性细胞浸润,非EAT对照组大鼠甲状腺未见明显炎性细胞浸润。EAT组大鼠甲状腺的炎症反应重于EAT+CsA组,诱发EAT的2组甲状腺的炎症反应随碘摄入量的增加而加重。(2)EAT组和EAT+CsA组的血清中自身抗体TG-Ab和TPO-Ab水平均高于对照组(P<0.05),EAT+CsA组的TG-Ab和TPO-Ab水平均低于EAT组,2组自身抗体水平亦随着碘摄入量的增加有升高趋势。(3)100倍碘水平的各组T4水平下降,各组的血清T3含量比较差异无统计学意义。结论增加碘的摄入量会明显加重EAT的炎症反应,促进EAT的形成和发展;CsA对EAT的形成及甲状腺自身抗体的产生有一定的抑制作用,碘过量可以拮抗CsA的这种作用,且随碘摄入量的增加拮抗效应增强;碘摄入过多可以抑制甲状腺激素的合成和释放。
Objective To study te supression of Cyclosporin A in the development of experimental autoimmune thyroiditis（EAT） that resisted by iodine and then to further understand the role of iodine in the pathogensis of autoimmune thyroiditis（AT）. Methods EAT model was established in rats of EAT group and CsA-treatment group with the different iodine intake levels by immunization with thyroglobulin of porcine. The rats of CsA-treatment group were injected with the CsA 5 mg/（kg·d）through the abdomen on the clay 10 after the first immunization. The rats of non-EAT control group were not immunized. Then the pathological changes and infiltration of lymphocyte in thyroid tissue of rats were observed. The leel of TG-Ab, TPO-Ab, T3 and T4 in the serum of rats were detectecd by the method of radioimmuoassay（RIA）. Results （1）The thyroid tissues of EAT group and CsA-treatment group were infiltrated by lymphocyte and the more intake of iodine, the more serious the inflammation in the thyroid tissue was. But there was almost no infiltration of lymphocytes in thyroid tissue in the every non-EAT control group. At the same level of iodine intake, the inflammation of rats in EAT group was more serious than that of rats in CsA-treatment group. （2）The level of serum TG-Ab and TPO-Ab in EAT group and CsA-treatment group was significantly higher than that of non-EAT control group（P 〈 0.05）. The serum TG-Ab and TPO-Ab of CsA-treat- ment group was lower that that of EAT group. The level of TG-Ab and TPO-Ab became higher with the increase of iodine intake. （3）The level of T4 was lower in the rats administered with 100 times iodine intake. There was no statistical significant difference among the groups in T3. Conclusion The increase of iodine intake could obviously aggravate the inflammation reaction of thyroid glands of rats with EAT and facilitate the development of EAT;CsA could suppress the development of EAT and production of autoantibody to a certain extent. But this action could be resisted by iodine excess. The increase of iodine intake enhanced effect of resistance; The high iodine intake could suppress the synthesis and release on thyroid hormone.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2005年第11期1315-1317,共3页
Chinese Journal of Public Health
基金
国家自然科学基金资助项目(20230330)
天津市高等学校科技发展基金项目(2004ZD08)
