ArticleMetabolic brain disease2025
Sodium butyrate alleviates spinal cord injury via inhibition of NLRP3/Caspase-1/GSDMD-mediated pyroptosis.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Emerging regenerative strategies for spinal cord injury: exosome-derived mechanisms and therapeutic insights.Frontiers in neuroscience · 2025Pooled it
- The impact of histone deacetylase inhibition on neurobehavioural outcomes in preclinical models of traumatic and non-traumatic spinal cord injury: a systematic review.Frontiers in immunology · 2025Pooled it
- A lesion-responsive ZIF-8/zinc-myricetin nano-biointerface remodels mitochondrial-immune crosstalk for spinal cord repair.Materials today. Bio · 2026Article
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
- Caspase-1 inhibition: mechanistic insights and comprehensive review of reported inhibitors to date.Inflammopharmacology · 2026Review
- Gut-derived signals regulating glial activation and secondary neuroinflammation after spinal cord injury: an evidence mapping and mechanistic framework.Frontiers in cellular neuroscience · 2026Review
- NLRP3 Inflammasome-Mediated Pyroptosis in Osteoporosis: Osteoimmune Mechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2025Review
- Effect of mitochondrial dysfunction on scar formation after spinal cord injury.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
NOD-like receptor protein 3 (NLRP3)/cysteinyl aspartate-specific proteinase 1 (Caspase-1)/gasdermin D (GSDMD)-mediated pyroptosis is linked to spinal cord injury (SCI) pathogenesis. The levels of short-chain fatty acids (SCFAs), especially butyric acid, are significantly altered after SCI. Sodium butyrate (NaB) has anti-inflammatory effects on SCI; however, its effect on pyroptosis is unknown. The aim of this study was to determine the role of NaB in SCI functional recovery and its effect on NLRP3/Caspase-1/GSDMD-mediated pyroptosis. SCI model rats were established using aneurysm clips. After SCI, rats were administered NaB (300 mg/kg) via gavage. SCFAs in faeces were measured using gas chromatography-mass spectrometry. Motor function recovery was assessed using cylinder rearing and grooming tests. Histopathological analysis was performed using haematoxylin-eosin staining, transmission electron microscopy, and terminal deoxynucleotidyl transferase dUTP nick-end labelling. The expression of proteins associated with pyroptosis signalling pathways was analysed using enzyme-linked immunosorbent assay, western blotting, and immunohistochemistry. SCFAs levels, particularly butyric acid, significantly decreased after SCI. NaB treatment promoted forelimb motor function recovery and attenuated pathological SCI. NaB also decreased spinal pro-inflammatory factors (interleukin-18 and interleukin-1β) and downregulated pyroptosis-related proteins, including NLRP3, apoptosis-associated speck-like protein, Caspase-1, and GSDMD. NaB inhibits NLRP3/Caspase-1/GSDMD-mediated neuronal pyroptosis and inflammation, exerting protective and therapeutic effects in SCI, suggesting NaB as an effective SCI treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.