地塞米松对甲状腺相关眼病眼眶成纤维细胞ICAM-1表达的影响

Effect of Dexamethasone on Expression of Intercellular Adhesion Molecule-1 in Orbital Fibroblasts from Thyroid Associated Ophthalmopathy

目的探讨地塞米松对甲状腺相关眼病(TAO)眼眶成纤维细胞(OF)细胞间粘附分子(ICAM-1)表达的影响。方法取10例TAO患者和5例正常对照的眼眶脂肪组织与眼外肌,体外培养OF,在培养基中分别加入10-6m o l/L地塞米松、300 U/mL干扰素-γ(IFN-γ)或10-6m o l/L地塞米松与300 U/mL IFN-γ的混合液,作用72 h,用流式细胞仪检测OF上ICAM-1的表达水平。结果体外培养的OF均表达ICAM-1,TAO患者的表达量高于正常对照者(P<0.05)。IFN-γ促进OF表达ICAM-1,地塞米松不仅抑制OF表达ICAM-1,而且能抑制IFN-γ诱导的ICAM-1表达。结论TAO患者OF表达ICAM-1增强可能是促进眶内炎症发生的原因之一,糖皮质激素发挥治疗作用的可能机制之一是其抑制OF表达ICAM-1以及IFN-γ诱导的ICAM-1表达。

Objective To investigate the effects of dexamethasone （DEX） on the expression of intercellular adhesion molecule-1 （ICAM-1） in orbital fibroblasts （OF） from patients with thyroid associated ophthalmopathy （TAO）. Methods OFs from 10 patients with TAO and from 5 normal control subjects were cultured in vitro. OFs were incubated with DEX, IFN-γ or DEX and IFN-γ compound for 72 hours. Flow cytometry analyses were performed to determine ICAM-1 expression. Results Banal ICAM-1 expression in OFs from TAO was significantly higher than that in the controls. DEX （10^-6 mol/L） inhibited expression of ICAM-1. IFN-γ （300 U/ mL） stimulated ICAM-1 expression significantly, which was inhibited by DEX （10^-6 mol/L）. Conclusion ICAM- 1 plays an important role in the pathogenesis of TAO. DEX not only inhibits ICAM-1 expression, but also inhibits IFN-γ-induced ICAM-1 expression on cultured OF in vitro. This may be part of the mechanism by which glucocorticoid has efficacy in the treatment of TAO.