ArticleBrain and behavior2026
Lipopolysaccharide Upregulates Neuroinflammation, Oxidative Stress Responses, and Peroxiredoxins in Depression Models.
Article in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Molecular Signaling Pathways in Depression and Neuroinflammation: Focus on New Pathophysiological Proteins and Therapeutic Compounds.Antioxidants (Basel, Switzerland) · 2026Review
- From Xenobiotic Exposure to Neuroinflammation: Mechanisms Linking Lipopolysaccharide Signaling to Depressive-like Behavior.Journal of xenobiotics · 2026Review
- Preventive Effects of Probiotic Formula on Metabolic Stress Associated Physical Fatigue in Forced Swimming and LPS-Induced Mouse Models.Journal of microbiology and biotechnology · 2026Article
- Lipopolysaccharide Upregulates Neuroinflammation, Oxidative Stress Responses, and Peroxiredoxins in Depression Models.Brain and behavior · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
introductionDepression is a chronic psychiatric disorder and belongs to one of the leading causes of suicide worldwide. Peroxiredoxins (Prdxs) play a critical role in scavenging excess reactive oxygen species (ROS) and mitigating oxidative stress. However, the role and underlying mechanisms of Prdxs in depression have not been fully illustrated.
methodsWe carried out lipopolysaccharide (LPS)-induced ICR depression mice and BV2 cell inflammation models. Seven days after LPS-induction, behaviors in ICR mice were assessed by open field test (OFT), sucrose preference test (SPT), and forced swim test (FST), and inflammatory factors levels in serum were quantified via ELISA. The expression levels of Prdxs were evaluated using immunohistochemistry (IHC), western blotting (WB), and RT-qPCR. In LPS-induced BV2 cells, inflammatory factor levels in the supernatant were measured by ELISA. Nitric oxide (NO) levels were detected by biochemical assay. ROS levels were detected via fluorescence signal intensity. Prdxs expression levels were analyzed using WB and RT-qPCR.
resultsIn LPS-induced ICR mice serum and BV2 cells supernatant, interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and transforming growth factor-beta1 (TGF-β1) levels exhibited significant elevation (p < 0.05). In the hippocampus region of LPS-induced mice and LPS-induced BV2 cells, significant upregulation of Prdx1, Prdx2, Prdx4, and Prdx5 levels was observed (p < 0.05). The ROS and NO levels in LPS-induced BV2 cells also significantly increased (p < 0.05).
conclusionsThis study revealed that Prdx1, Prdx2, Prdx4, and Prdx5 were elevated in depression models, which might relate to the occurrence of neuroinflammation, coupled with upregulation of oxidative stress responses. This study provided new strategies for the treatment of depression.
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