N-乙酰半胱氨酸、还原型谷胱甘肽及地塞米松对人甲状腺细胞氧化应激的影响

Effects of N-acetylcysteine, glutathione, and dexamethasone on oxidative stress of human thyrocyte

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.