摘要
取人甲状腺腺瘤旁正常甲状腺组织进行细胞培养,以1 000 IU/ml干扰素γ(IFN-γ)+10ng/ml肿瘤坏死因子α(TNF-α)、1 mmol/L N-乙酰半胱氨酸(NAC)、1 mmol/L还原型谷胱甘肽(GSH)、10μmol/L地塞米松(DEX)孵育,测定细胞培养上清液中丙二醛、谷胱甘肽过氧化物(GSH-Px)和总超氧化物歧化酶(SOD)水平.结果显示,IFN-y+TNF-α处理组与对照组比较,丙二醛水平显著增加(P<0.05),GSH-Px和SOD活性显著下降(P<0.05);经NAC、GSH和DEX干预后,IFN-γ+TNF-α刺激的丙二醛水平均显著下降(P<0.05),GSH-Px和SOD活性显著升高(P<0.05).这些结果表明IFN-γ和TNF-α可以诱导甲状腺细胞发生氧化应激,NAC、GSH及DEX可通过增加细胞GSH-Px、SOD活性和降低丙二醛含量来拮抗氧化应激反应.
[Summary] The human thyroid epithelium cells were obtained from normal para-adenoma tissues of patients with thyroid adenoma or nodule.Cells were treated with 1 000 IU/ml interferon-γ (IFN-γ) + 10 ng/ml tumor necrosis factor-α (TNF-α),1 mmol/L N-acetylcysteine (NAC),1 mmol/L glutathione (GSH),and 10 μmol/L dexamethasone (DEX) respectively.Malondialdehyde(MDA),glutathioneperoxidase(GSH-Px),and superoxidedismutase(SOD) levels in the cell supernatant were measured.The results showed that IFN-γ+TNF-α significantly increased MDA level (P〈0.05) while decreased GSH-Px and SOD levels (P〈0.05).After NAC,GSH,and DEX intervention,MDA levels all were significantly lowered (all P〈0.05) while GSH-Px and SOD levels were significantly increased compared with IFN-γ+TNF-α stimulation(all P〈0.05).These results suggest that IFN-γ and TNF-α can induce oxidative stress in the human thyrocyte,and this effect is antagonized by NAC,GSH,and DEX via increasing GSH-Px,SOD activity and decreasing MDA content.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
2015年第1期71-74,共4页
Chinese Journal of Endocrinology and Metabolism
基金
南京市医学科技发展项目基金(ZKX12023)