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目的研究瘦素在诱发实验性自身免疫性甲状腺炎(EAT)形成中的影响。方法采用C57BL/6J小鼠在外源性瘦素干预下诱发EAT,观察小鼠甲状腺组织病理改变、淋巴细胞增殖水平、脾细胞培养上清中IFN-γ和IL-4水平以及血清中甲状腺过氧化物酶抗体(TPO-Ab)、甲状腺球蛋白抗体(Tg-Ab)和瘦素水平。结果小鼠经外源性瘦素干预后,其血清中瘦素水平高于EAT组和对照组,实验性自身免疫性甲状腺炎的发病率和甲状腺组织中炎细胞浸润程度也较直接诱发EAT组明显增高。诱发EAT两实验组间比较,脾细胞增殖水平未见明显差异,但瘦素干预组脾细胞培养上清中IFN-γ水平较EAT组明显升高(P=0.000),而IL-4水平则低于EAT组(P=0.000)。两实验组小鼠血清中TPO-Ab和Tg-Ab水平均明显高于未诱发EAT对照组,但两组间比较均未见明显差异。结论瘦素的前炎症作用在实验性自身免疫性甲状腺炎的发生、发展中有重要免疫调节作用。
Objective To study the effect of leptin on the induction of experimental autoimmune thyroiditis (EAT). Methods The EAT was induced by exogenous leptin in C57BL / 6J mice. The pathological changes of thyroid tissue, the proliferation of lymphocytes, the levels of IFN-γ and IL-4 in the culture supernatant of spleen cells and the levels of thyroid peroxidation Enzyme-linked immunosorbent (TPO-Ab), thyroglobulin antibody (Tg-Ab) and leptin levels. Results After exogenous leptin intervention, the leptin level in serum was higher than that in EAT group and control group. The incidence of experimental autoimmune thyroiditis and inflammatory cell infiltration in thyroid tissue were also significantly higher than those in EAT group Significantly higher. There were no significant differences in the proliferation of spleen cells between two experimental groups induced by EAT, but the level of IFN-γ in splenocyte culture supernatant of the leptin intervention group was significantly higher than that of EAT group (P = 0.000), while the level of IL-4 Lower than EAT group (P = 0.000). The serum levels of TPO-Ab and Tg-Ab in the two experimental groups were significantly higher than those in the control group without EAT, but no significant difference was found between the two groups. Conclusion The pro-inflammatory effect of leptin plays an important immunomodulatory role in the development and progression of experimental autoimmune thyroiditis.