ArticleBMC genomics2023
Identification of biomarkers and therapeutic targets related to Sepsis-associated encephalopathy in rats by quantitative proteomics.
Article in BMC genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Cerebrospinal Fluid Hemopexin as a Candidate Biomarker for Secondary Sepsis and In-Hospital Outcome After Spontaneous Intracerebral Hemorrhage: An Exploratory Translational Proteomics Study.Neurocritical care · 2026Article
- Exploring the Proteomic Landscape of Cochlear Implant Trauma: An iTRAQ-Based Quantitative Analysis Utilizing an Ex Vivo Model.Journal of clinical medicine · 2025Article
- PI3K/Akt pathway and neuroinflammation in sepsis-associated encephalopathy.Open medicine (Warsaw, Poland) · 2025Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSepsis-associated encephalopathy (SAE) is a common and severe complication of sepsis. While several studies have reported the proteomic alteration in plasma, urine, heart, etc. of sepsis, few research focused on the brain tissue. This study aims at discovering the differentially abundant proteins in the brains of septic rats to identify biomarkers of SAE.
methodsThe Prague-Dawley rats were randomly divided into sepsis (n = 6) or sham (n = 6) groups, and then the whole brain tissue was dissected at 24 h after surgery for further protein identification by Quantitative iTRAQ LC-MS/MS Proteomics. Ingenuity pathway analysis, Gene ontology knowledgebase, and STRING database are used to explore the biological significance of proteins with altered concentration.
resultsAmong the total of 3163 proteins identified in the brain tissue, 57 were increased while 38 were decreased in the sepsis group compared to the sham group. Bioinformatic analyses suggest that the differentially abundant proteins are highly related to cellular microtubule metabolism, energy production, nucleic acid metabolism, neurological disease, etc. Additionally, acute phase response signaling was possibly activated and PI3K/AKT signaling was suppressed during sepsis. An interaction network established by IPA revealed that Akt1, Gc-globulin, and ApoA1 were the core proteins. The increase of Gc-globulin and the decrease of Akt1 and ApoA1 were confirmed by Western blot.
conclusionBased on the multifunction of these proteins in several brain diseases, we first propose that Gc-globulin, ApoA1, PI3K/AKT pathway, and acute phase response proteins (hemopexin and cluster of alpha-2-macroglobulin) could be potential candidates for the diagnosis and treatment of SAE. These results may provide new insights into the pathologic mechanism of SAE, yet further research is required to explore the functional implications and clinical applications of the differentially abundant proteins in the brains of sepsis group.
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