ArticleEuropean journal of medical research2025
Molecular hydrogen-mediated SIRT1 activation alleviates sepsis-associated encephalopathy by promoting mitophagy.
Article in European journal of medical research, 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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1 citing paper in PubMed.
- SIRT1 Activation Ameliorates Neuroinflammation and Cognitive Impairment in a Murine SAE Model and is Associated with the Nrf2/GPX4 Pathway.Neurochemical research · 2026Article
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12 authors.
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Abstract
backgroundSepsis-associated encephalopathy (SAE) constitutes a major determinant of sepsis-related mortality across acute and survivorship phases. While molecular hydrogen (H₂) exhibits neuroprotective capacities in SAE, its precise mechanistic underpinnings remain unresolved. This study investigates the protection of SAE by H
methodsSAE was modeled in mice via cecal ligation and puncture (CLP). The cognitive abilities of mice were evaluated via behavioral tests (Morris water maze), observation of the pathological morphology of brain tissues (HE staining), and observation of neuronal cell structure (Nissl staining). Proteomics was employed to explore the specific mechanism by which hydrogen regulates mitophagy. Western blotting, immunofluorescence, and electron microscopy were used to quantify the dynamic changes of sirtuin 1 (SIRT1) and mitophagy during SAE. In addition, an SIRT1 inhibitor (EX527) was utilized to observe its effects on hydrogen treatment and mitophagy.
resultsInhalation of 2% hydrogen significantly enhanced the 7-day survival rate of septic mice (from 50 to 75%, P < 0.01) and improved cognitive performance in the Morris water maze, as evidenced by increased platform crossings (P < 0.05) and reduced escape latency. Hydrogen treatment upregulated SIRT1 expression and promoted PINK1/Parkin-mediated mitophagy, leading to reduced phosphorylation of STING, decreased levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), and suppressed neuronal apoptosis in the hippocampal CA1 region. These protective effects were reversed by the SIRT1 inhibitor EX527.
conclusionsThis study demonstrates that inhalation of 2% H2 exerts significant protective effects against SAE, in which SIRT1 plays a pivotal role by modulating PINK1-dependent mitophagy, thereby ameliorating neuroinflammation and neuronal apoptosis. By rescuing mitophagy deficits, SIRT1 targeting merits clinical exploration for SAE.
trial registrationNot applicable.
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