Journal of inflammation researchOct 14, 2025

Apigenin may reduce inflammation and cell death while helping recovery by boosting damaged mitochondria cleanup in rats with spinal cord injury

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Jun 27, 2026

Abstract

Essence

Apigenin improved recovery markers after experimental spinal cord injury in rats by promoting and suppressing microglial .

Evidence

This preclinical rat spinal cord injury study used behavioral, electrophysiological, histological, ELISA, qPCR, immunofluorescence, and JC-1 assays, with Mdivi-1 reversal and Urolithin A mimicry supporting a mitophagy-mediated mechanism.

Caveat

The evidence is limited to an experimental rat model and mechanistic assays, so it does not show human spinal cord injury efficacy.

Simplified

BACKGROUND: Secondary damage following spinal cord injury (SCI) is closely associated with and mitochondrial dysfunction. Apigenin (API), a natural flavonoid, possesses notable anti-inflammatory and antioxidant properties. However, whether API can inhibit microglial pyroptosis via the 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.

Key numbers

10 mg/kg and 50 mg/kg

Motor Function Improvement

treatment groups showed higher BBB scores starting from day 14 post-injury.

TNF-α and IL-1β

Reduction in Inflammatory Cytokines

Measured levels of TNF-α and IL-1β in spinal cord tissue post-SCI.

increased

Enhanced

Quantification of in post-treatment with .

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Apigenin may reduce inflammation and cell death while helping recovery by boosting damaged mitochondria cleanup in rats with spinal cord injury

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