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初诊未用药精神分裂症患者 TNF-α 与氧化应激状态的相互作用。

Interaction between TNF-α and oxidative stress status in first-episode drug-naïve schizophrenia.

机构信息

The First Clinical Medical College, Nanjing Medical University, Nanjing, China; Department of Neurology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.

Qingdao Mental Health Center, Qingdao University, Qingdao, China.

出版信息

Psychoneuroendocrinology. 2020 Apr;114:104595. doi: 10.1016/j.psyneuen.2020.104595. Epub 2020 Jan 30.

DOI:10.1016/j.psyneuen.2020.104595
PMID:32036201
Abstract

There has been evidence that the disturbances of TNF-α and the oxidative stress (OxS) status are involved in the mechanism of schizophrenia. However, the results of their levels in schizophrenia are still controversial, and their interactions have not yet been examined, especially in first-episode drug-naïve (FEDN) patients. We therefore applied Enzyme-linked immunosorbent assays (ELISAs) method to compare peripheral blood serum TNF-α, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA) levels in 119 FEDN patients with schizophrenia and 135 healthy controls. We found that TNF-α and MDA were higher, whereas GSH-Px was lower, in FEDN patients with schizophrenia compared to healthy controls (TNF-α, 2.21 ± 0.33 vs. 2.11 ± 0.36, Bonferroni p = 0.04; MDA, 2.95 ± 0.87 vs. 2.68 ± 0.76, Bonferroni p = 0.04, GSH-Px, 177.33 ± 28.84 vs. 188.32 ± 29.34, Bonferroni p = 0.03). Furthermore, TNF-α levels had an independent positive association with negative symptoms (r = 0.37, Bonferroni p < 0.001). Finally, GSH-Px levels were negatively associated with the presence of schizophrenia (B =-0.014, Wald statistic = 9.22, p = 0.002, 95 %CI = 0.97-0.99), while the interaction of TNF-α with MDA was a risk factor for schizophrenia (B = 0.22, Wald statistic = 10.06, p = 0.002, 95 %CI = 1.09-1.43). Our results suggest that TNF-α and disturbance of oxidative stress status as well as their interaction may be involved in the pathophysiology of schizophrenia.

摘要

有证据表明,TNF-α 的紊乱和氧化应激(OxS)状态与精神分裂症的发病机制有关。然而,它们在精神分裂症中的水平的结果仍然存在争议,并且它们的相互作用尚未被检测到,特别是在首发未经药物治疗的(FEDN)患者中。因此,我们应用酶联免疫吸附测定(ELISA)方法比较了 119 例 FEDN 精神分裂症患者和 135 例健康对照组的外周血清 TNF-α、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)和丙二醛(MDA)水平。我们发现,与健康对照组相比,FEDN 精神分裂症患者的 TNF-α 和 MDA 更高,而 GSH-Px 更低(TNF-α,2.21 ± 0.33 比 2.11 ± 0.36,Bonferroni p = 0.04;MDA,2.95 ± 0.87 比 2.68 ± 0.76,Bonferroni p = 0.04,GSH-Px,177.33 ± 28.84 比 188.32 ± 29.34,Bonferroni p = 0.03)。此外,TNF-α 水平与阴性症状呈独立的正相关(r = 0.37,Bonferroni p < 0.001)。最后,GSH-Px 水平与精神分裂症的存在呈负相关(B =-0.014,Wald 统计量 = 9.22,p = 0.002,95 %CI = 0.97-0.99),而 TNF-α 与 MDA 的相互作用是精神分裂症的危险因素(B = 0.22,Wald 统计量 = 10.06,p = 0.002,95 %CI = 1.09-1.43)。我们的结果表明,TNF-α 和氧化应激状态的紊乱以及它们的相互作用可能参与了精神分裂症的病理生理学。

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