ArticleCNS neuroscience & therapeutics2025
Optimized Mouse Model of Sepsis-Associated Encephalopathy: A Rational Standard Based on Modified SHIRPA Score and Neurobehaviors in Mice.
Article in CNS neuroscience & therapeutics, 2025. 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.
- Endothelial-specific Ezh2 deficiency exacerbates blood-brain barrier dysfunction and neuroinflammation in sepsis-associated encephalopathy.Journal of neuroinflammation · 2026Article
- Hypothalamic arcuate microglia in sepsis: AgRP circuit engagement and ARHGAP24-dependent remodeling.Journal of neuroinflammation · 2026Article
- Capsaicin attenuates sepsis‑associated encephalopathy by inhibiting neuroinflammation and apoptosis whilst activating mitophagy through the BNIP3/NIX pathway.Molecular medicine reports · 2025Article
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Authors and funding
9 authors.
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Abstract
backgroundSepsis-associated encephalopathy (SAE), a severe neurological disorder, is marked by widespread brain dysfunction. At present, there is no universally accepted criterion for diagnosing SAE in animal models. This study proposes a standardized evaluation method for SAE in mice, addressing inconsistencies in current research.
methodUsing a cecal ligation and puncture (CLP) model to induce sepsis, we assessed the physiological status of mice with a modified SHIRPA score to differentiate SAE from non-SAE, validating our findings through various behavioral tests and evaluations of neuroinflammation and neuronal damage.
resultsOur findings revealed that the conventional mild-moderate-severe categorization of SHIRPA was insufficient for distinguishing between SAE and non-SAE. To enhance differentiation, we classified mice based on the median modified SHIRPA score, validating this approach through behavioral tests including the Y-maze, three-chamber social test, and open field test. This method effectively identified neurological impairments in septic mice. Further validation involved assessing neuronal damage, neuroinflammation, the Morris water maze, and long-term potentiation (LTP) in the hippocampal CA1 region. Results indicated that mice in the up-Median group exhibited greater neuroinflammation, neuronal injury, and cognitive deficits compared to the down-Median group.
conclusionsThis study establishes a reliable evaluation method for SAE in murine models, facilitating improved differentiation between SAE and non-SAE. Such advancements will enhance our understanding of the pathogenesis of SAE and guide more effective treatment strategies.
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