ArticleJournal of molecular neuroscience : MN2025
Proteomic Profiling and Therapeutic Targeting of Oxidative Stress in Autoimmune Encephalitis.
Article in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Identification and validation of selenium metabolism-related genes in lung adenocarcinoma prognosis using bioinformatics analysis.Frontiers in genetics · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Autoimmune encephalitis (AE) is an immune-mediated non-infectious disease, and novel and robust biomarkers are needed to improve the diagnosis and prognostic outcomes of AE. Oxidative stress is a ubiquitous cellular process causing damage to various biological molecules. The aim of our study was to understand the clinical implication and mechanism underlying oxidative stress in AE. Liquid chromatography-mass spectrometry analysis was conducted on the serum of eight patients with AE and seven healthy controls, and oxidative stress was characterized. Experimental autoimmune encephalitis (EAE) models were established in C57BL/6 and SJL mice for investigation of the therapeutic effect and mechanism of anti-oxidative stress N-acetylcysteine (NAC). We provided proteomic landscape in the serum of AE and identified antioxidant ALB, APOE, GPX3, and SOD3 as serum diagnostic markers of AE. The antioxidant markers were lowly expressed both in the serum of AE patients and central nervous system (CNS) of EAE mice. NAC administration improved clinical signs and motor function and alleviated nerve injury of EAE mice as well as lowered oxidative stress (decreased MDA content and ROS accumulation and elevated SOD activity and GSH content). ALB, APOE, GPX3, and SOD3 expressions were elevated by NAC in the CNS of EAE mice. Moreover, NAC reduced tissue-resident CD4
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