Association between elevated serum matrix metalloproteinase-2 and tumor necrosis factor-α, and clinical symptoms in male patients with treatment-resistant and chronic medicated schizophrenia

Author:

Yang Haidong1,Peng Ruijie2,Yang Man1,Zhang Jing1,Shi Zhihui1,Zhang Xiaobin2

Affiliation:

1. The Fourth People’s Hospital of Lianyungang, The Affiliated KangDa College of Nanjing Medical University

2. Institute of Mental Health, The Affiliated Guangji Hospital of Soochow University

Abstract

Abstract Background: Inflammation has an important role in the pathogenesis of schizophrenia. The aim of this study was to investigate the levels of tumor necrosis factor (TNF) and matrix metalloproteinase-2 (MMP-2) in male patients with treatment-resistant schizophrenia (TRS) and chronic medicated schizophrenia (CMS), and the relationship with psychopathology. Methods: The study enrolled 31 TRS and 49 CMS male patients, and 53 healthy controls. Serum MMP-2 and TNF-a levels were measured by the Luminex liquid suspension chip detection method. Positive and Negative Syndrome Scale (PANSS) scores were used to evaluate symptom severity and Repeatable Battery for the Assessment of Neuropsychological Status was used to assess cognitive function. Results: Serum TNF-a and MMP-2 levels differed significantly between TRS, CMS and healthy control patients (F=4.289, P=0.016; F=4.682, P=0.011, respectively). Bonferroni correction demonstrated that serum TNF-a levels were significantly elevated in CMS patients (P=0.022) and MMP-2 levels were significantly higher in TRS patients (P=0.014) compared to healthy controls. In TRS patients, TNF-a was negatively correlated with age (r=-0.435, P=0.015) and age of onset (r=-0.409, P=0.022). In CMS patients, MMP-2 and TNF-a were negatively correlated with PANSS negative and total scores, and TNF-a was negatively correlated with PANSS general psychopathology scores (all P<0.05). MMP-2 levels were positively correlated with TNF-a levels (P<0.05), but not with cognitive function (P>0.05). Conclusion: The results indicate the involvement of inflammation in the etiology of TRS and CMS. Further studies are warranted.

Publisher

Research Square Platform LLC

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