摘要
目的 研究雌激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 10周龄Wistar大鼠进行双侧卵巢切除术后采用同种属SD大鼠甲状腺球蛋白 (Tg)免疫诱发EAT。病理切片HE染色观察甲状腺炎症反应。采用放免方法测定血清中E2 、PRL水平。间接酶联免疫吸附实验 (ELISA )测定血清Tg抗体 (TgAb)水平。逆转录 聚合酶链反应 (RT PCR)检测甲状腺组织中γ 干扰素 (IFN γ)、白细胞介素 10 (IL 10 )mRNA的表达水平。结果 大鼠切除双侧卵巢后 ,其血清中雌二醇 ( 17.60± 1.0 2 )pmol/L和PRL( 2 .45± 0 .15 ) μg/L水平明显低于未切除卵巢组〔分别为 ( 5 8.5 6± 6.99) pmol/L和 ( 3 .2 2± 0 .17) μg/L〕(均P <0 .0 1) ,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均较未切除卵巢直接诱发EAT组明显减轻 ,甲状腺组织中IFN γmRNA的表达水平 ( 0 .87± 0 .0 3 )较未切除卵巢直接诱发EAT组 ( 0 .99± 0 .0 0 )明显下降 (P <0 .0 5 ) ,而IL 10mRNA的表达水平 ( 0 .98± 0 .0 1)则高于未切除卵巢直接诱发EAT组 ( 0 .83± 0 .0 5 )。诱发为EAT的两组大鼠血清TGAb平均水平 ( 1.3 9± 0 .0 3 )明显高于非诱发EAT对照组的平均水平 ( 0 .18± 0 .0 0 )(P <0 .0 1)。
Objective To observe the effects of estradiol-17β (E 2-17β) on the induction of experimental autoimmune thyroiditis (EAT). Methods Ten-week old female Wistar rats were ovariectomized (OVX). EAT of Wistar rats was induced by immunization with thyroglobulin (Tg) from SD rats in the presence of complete Freund′s adjuvant. Thyroiditis was pathologically evaluated by HE staining. E 2-17β and PRL levels were measured by RIA, anti-Tg antibody (TgAb) was detected by ELISA, and interferon (IFN)-γ, interleukin (IL)-10 mRNA in thyroid were assayed by RT-PCR. Results The serum level of E 2-17β (17.60±1.02)pmol/L and PRL (2.45±0.15)μg/L were much lower in OVX rats than intact rats 〔(58.56±6.99)pmol/L and (3.22±0.17)μg/L, respectively〕 (both P<0.01). The OVX group showed a significant reduction in extent of inflammatory cell infiltration and incidence of EAT and the expression level of IFN-γ mRNA (0.99±0.00 vs 0.87±0.03, P<0.05) following the increment of IL-10 mRNA (0.83±0.05 vs 0.98±0.01,P<0.05).Meanwhile,themeanlevel of TgAb was higher in the EAT groups (1.39±0.03) than that in the non-EAT groups (0.18±0.00) (P<0.01). Conclusion E 2-17β is a key factor for the development of EAT and decreased serum level of the E 2-17β may be beneficial for the amelioration of EAT.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
2004年第2期151-154,共4页
Chinese Journal of Endocrinology and Metabolism
基金
国家自然科学基金资助项目 (30 0 70 676)
