地塞米松对甲状腺细胞炎症反应的影响  

Effect of dexamethasone on inflammatory response of thyrocytes

作　　者：冯田田[1] 胡蕴[2] 陈婧[2] 程程[2] 何珂[2] 毛晓明[2] 

机构地区：[1]连云港市妇幼保健院 [2]南京医科大学附属南京医院(南京市第一医院)内分泌科,210006

出　　处：《中华内分泌代谢杂志》2014年第6期507-510,共4页Chinese Journal of Endocrinology and Metabolism

摘　　要：目的 研究地塞米松对甲状腺细胞炎症反应的影响.方法 取Graves病患者甲状腺组织,提取原代甲状腺细胞进行体外培养,分别加入γ-干扰素（IFN-γ）和肿瘤坏死因子α（TNF-α）刺激细胞,然后培养于地塞米松中,分为4组,即对照组、地塞米松组、TNF-α＋ IFN-γ组和地塞米松＋TNF-α＋IFN-γ组.用酶联免疫吸附法检测细胞上清液中干扰素诱导蛋白10（CXCL10）和单核细胞趋化蛋白1（CCL2）浓度.提取细胞全蛋白,Western印迹法检测GSK-3β、P50和P100蛋白浓度变化.结果 MTT结果显示10-5mmol/L地塞米松为最佳作用浓度.TNF-α＋IFN-γ组CXCL10水平明显高于对照组和地塞米松组（P＜0.01）;地塞米松＋TNF-α＋IFN-γ组与TNF-α＋ IFN-γ组相比CXCL10水平无显著差异（P＞0.05）.TNF-α＋IFN-γ组CCL2水平明显高于对照组和地塞米松组（P＜0.01）.地塞米松＋TNF-α＋IFN-γ组与TNF-α＋IFN-γ组相比,CCL2水平降低（P＜0.05）.TNF-α＋IFN-γ与对照组相比,GSK-3β、P100蛋白表达增多,地塞米松处理可以降低＋TNF-α＋IFN-γ诱导的蛋白表达.结论 TNF-α和IFN-γ能刺激甲状腺细胞分泌CXCL10及CCL2,介导甲状腺免疫炎症的发生.地塞米松可降低CCL2水平,减轻体液免疫反应.地塞米松对CXCL10无明显变化.地塞米松使NF-κB相关蛋白GSK-3β、P100表达减少,抑制NF-KB信号通路激活,抑制炎症反应.Objective To explore the impact of dexamethasone on inflammatory response of thyrocytes.Methods Primary thyrocytes were extracted from thyroid tissue of patients with Graves＇ disease.The cells were stimulated with interferon-γ （IFN-γ） and tumor necrosis factor-α （TNF-α）,and cultured in dexamethasone.Thyrocytes were divided into 4 groups：control group,dexamethasone group,TNF-α ＋ IFN-γ group,and dexamethasone＋TNF-α＋IFN-γ group.Interferon-γ-induced protein 10 （CXCL10） and CCL2 in supernatant of cell cultured in 4 groups were detected by enzyme-linked immunosorbent assay.Cell protein in 4 groups was extracted and GSK-3β,P50,and P100 protein were detected by Western blotting.Results MTT assay demonstrated that 10-5 mmol/L concentration of dexamethasone was optimal for cell culture.The CXCL10 level in TNF-α＋IFN-γ group was higher than that in the control group and dexamethasone group （P＜0.01）,but no difference was found between dexamethasone＋TNF-α＋IFN-γgroup and TNF-α＋IFN-γgroup（P＞0.05）.The CCL2 level in TNF-α＋IFN-γ group was higher than that in control group and dexamethasone group（P＜0.01）.There was a significant lowering of CCL2 level in dexamethasone ＋ TNF-α ＋ IFN-γgroup compared with TNF-α ＋ IFN-γ group （P ＜ 0.05）.The expression of GSK-3β and P100 protein was increased in TNF-α ＋ IFN-γgroup compared with control group.The expression of GSK-3β and P100 protein was lower in dexamethasone＋TNF-α ＋ IFN-γ group than that in TNF-α ＋ IFN-γ group.Conclusion TNF-α ＋ IFN-γ could stimulate the secretion of CXCL10 and CCL2 in thyrocytes and thus activate the inflammatory response.Dexamethasone could reduce CCL2 secretion.Dexamethasone had little effect on CXCL10.Dexamethasone could reduce GSK-3β and P100 expressions,and inhibit the activation of NF-κB signaling pathway and thus the inflammatory response.

关 键 词：甲状腺细胞 炎症反应 地塞米松 格雷夫斯病 

分 类 号：R581.4[医药卫生—内分泌]