碘对环孢霉素A抑制免疫性甲状腺炎拮抗作用
Effect of cyclosporin A on suppressing develoment of autoimmune thyroiditis resisted by iodine
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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.Abstract:Objective To studyte supression of Cyclosporin Ain the development of experimental autoimmune thyroiditis(EAT)thatresisted by iodine and then tofurther understand the role of iodine in the pathog ensis of autoimmune thyroiditis(AT).Methods EATmodel was established in rats of EATgroup and CsA-treatmentgroup with the differentiodine intake levels by immunization with thyrog lobulin of porcine.The rats of CsA-treatmentgroup were injected with the CsA 5 mg/(kg·d)throug h the abdomen on the day 10 after the firstimmunization.The rats of non-EATcontrol group were notimmunized.Then the pathological changes and infiltration of lymphocyte in thyro id tissue of rats were obser ved.The leel of TGAb, TPO-Ab, T3 and T4 in the serum of rats were detectecd by the method of radioimmuo assay(RIA).Results (1) The thyro id tissues of EATgroup and CsA-treatmentgroup were infiltrated by lymphocy te and the more intake of iodine, the more serious the inflammation in the thyro id tissue was.Butthere was almostno infiltration of lymphocytes in thyroid tissue in the every non-EATcontrol group.Atthe same level of iodine intake, the inflammation of rats in EATgroup was more serious than thatof rats in CsA-treatmentgroup.(2)The level of serum TG-Ab and TPO-Ab in EATgroup and CsA-treatmentgroup was sig nificantly hig her than thatof non-EATcontrol group(P < 0.05).The serum TG-Ab and TPO-Ab of CsA-treatmentgroup was lower thatthatof EATgroup.The level of TG-Ab and TPO-Ab became higher with the increase of iodine intake.(3)The level of T4 was lowerin 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 EATand facilitate the developmentof EAT; CsA could suppress the develo pmentof EATand production of autoantibody to a certain extent.Butthis action could be resisted by iodine excess.The increase of iodine intake enhanced effectof resistance; The high iodine intake could suppress the sy nthesis and release on thyroid hormone.
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