ArticleFrontiers in toxicology2026
Botulinum toxin type E alleviates trigeminal neuropathic pain via modulation of the HIF-1α-NLRP3 pathway.
Article in Frontiers in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: While botulinum neurotoxin type E (BoNT/E) has been shown to have analgesic effects in previous studies, the underlying mechanisms mediating its therapeutic effects remain incompletely understood. This study investigated the involvement of the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome in the antinociceptive effects of BoNT/E in a rat model of trigeminal neuropathic pain. Methods: Neuropathic pain was induced in male Sprague-Dawley rats through inferior alveolar nerve (IAN) injury. Results: IAN injury significantly decreased air-puff thresholds, resulting in mechanical allodynia that persisted for up to 42 days. NLRP3 expression in the ipsilateral trigeminal ganglion (iTG) was significantly increased in the nerve-injured group on postoperative day (POD) 5. In contrast, subcutaneous administration of BoNT/E (6 or 10 U/kg) significantly attenuated mechanical allodynia and suppressed NLRP3 expression in the iTG on POD 5. Moreover, BoNT/E (10 U/kg) markedly reduced the elevated levels of inflammatory cytokines, including interleukin (IL)-1β, IL-18, tumor necrosis factor-alpha (TNF-α), and IL-6 in the iTG by IAN injury. The nerve-injured group also exhibited significant upregulation of hypoxia-inducible factor 1-alpha (HIF-1α) expression in the iTG, which was significantly decreased following BoNT/E (10 U/kg) treatment. Intraganglionic injection of PX-478, a HIF-1α inhibitor, similarly attenuated mechanical allodynia, downregulated NLRP3 expression, and decreased IL-1β, IL-18, TNF-α, and IL-6 levels in the iTG. Conclusion: Collectively, these findings demonstrate that modulation of the HIF-1α-NLRP3 pathway in the iTG plays a critical regulatory role in neuropathic pain development and suggest that BoNT/E may serve as a promising therapeutic strategy for managing chronic neuropathic pain.
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