摘要
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 influence of leptin on the induction of experimental autoimmune thyroiditis(EAT). Methods Female C57BL/6J mice were injected intraperitoneally with rmleptin or PBS starting 3 days before the induction of EAT. Histological severity of thyroid specimens was evaluated. The level of spleen lymphoeytes proliferative response and the concentration of the cytokines( IFN - γ and IL - 4) in the cell supernatants were measured. The serum levels of TPO - Ab , Tg - Ab and leptin were assayed. Results The serum level of leptin was higher in group treated with rmleptin than other two groups. The EAT group treated with rmleptin developed more severe thyroiditis compared with non - treated EAT group. Between two EAT groups , rmleptin did not alter spleen lymphocyte proliferative responses while rmleptin did increase IFN -γand reduce IL - 4 secretion in the cell supernatants. Meanwhile, high serum levels of TPO -Ab and Tg -Ab were presented in the experimental groups. Conclusion The character of proin flammatory of leptin contributes to the induction of EAT.
出处
《中国地方病防治》
2009年第1期1-4,共4页
Chinese Journal of Control of Endemic Diseases