ArticleJournal of inflammation research2025
Apigenin Suppresses NLRP3 Inflammasome Activation and Pyroptosis and Promotes Functional Recovery by Promoting Mitophagy in Experimental Spinal Cord Injured Rats.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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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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
2 citing papers in PubMed.
- Photobiomodulation‑Engineered Extracellular Vesicles Enhance Neural Differentiation via UFL1‑Mediated UFMylation in Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Unveiling the anti-cancer properties of apigenin via targeting different molecular signatures: A Review.Molecular biology reports · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Secondary damage following spinal cord injury (SCI) is closely associated with pyroptosis and mitochondrial dysfunction. Apigenin (API), a natural flavonoid, possesses notable anti-inflammatory and antioxidant properties. However, whether API can inhibit microglial pyroptosis via the mitophagy pathway, thereby exerting neuroprotective effects, remains unclear. This study aimed to elucidate the mechanism by which API mitigates post-SCI inflammatory responses through modulation of the mitophagy-NLRP3 axis. Methods: Neurological recovery was assessed using the Basso, Beattie, and Bresnahan scale, neuroelectrophysiological recordings, and histological analyses. The effects of API on NLRP3 inflammasome activation, reactive oxygen species (ROS) generation, and mitochondrial membrane potential were assessed using ELISA, quantitative PCR, immunofluorescence, and JC-1 staining. Results: API significantly improved locomotor function in SCI rats, reduced scar formation, and promoted axonal regeneration. Mechanistically, API downregulated NLRP3/ gasdermin D expression in microglia, reduced the release of inflammatory factors, and enhanced mitophagy. Notably, the protective effects of API were reversed by Mdivi-1 and mimicked by Urolithin A, confirming that mitophagy is the primary mechanism mediating API's anti-pyroptotic effects. Conclusion: API attenuates microglial pyroptosis and facilitates SCI repair by enhancing mitophagy-mediated clearance of damaged mitochondria and suppressing activation of the ROS/NLRP3 inflammasome pathway in rats. These findings provide important preclinical evidence supporting the development of multi-target neuroprotective strategies derived from natural compounds.
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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.