ArticleFrontiers in pharmacology2026
Acteoside alleviates slow transit constipation with attenuation of NLRP3 inflammasome activation and preservation of enteric neurons.
Article in Frontiers in pharmacology, 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: Slow transit constipation (STC) is characterized by delayed intestinal transit and impaired defecation, with enteric nervous system (ENS) injury and inflammatory dysregulation contributing to its pathogenesis. Acteoside (ACT), a natural phenylethanoid glycoside, has anti-inflammatory and neuroprotective properties. However, its therapeutic effect and mechanism in STC remain unclear. Methods: The effects of ACT were investigated in a loperamide (LOP)-induced STC-like mouse model. Intestinal motility, colonic morphology, and ENS integrity were evaluated by functional assays, hematoxylin and eosin (H&E) staining, and immunofluorescence. Transcriptomic analysis was performed to screen ACT-responsive inflammatory pathways. NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and cytokine production were assessed by Western blotting, enzyme-linked immunosorbent assay (ELISA), and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: ACT shortened defecation latency, increased fecal water content and pellet number, and improved intestinal propulsion. ACT also alleviated colonic histopathological injury, restored muscular layer thickness, preserved HuC/D-positive myenteric neurons, and increased PGP9.5-positive nerve fiber density. Transcriptomic analysis identified NLRP3-related inflammatory signaling within broader high-dose ACT-responsive transcriptional changes. At the molecular level, high-dose ACT reduced the protein levels of NLRP3, cleaved-caspase-1, and cleaved-interleukin-1β (IL-1β) expression and reduced IL-1β, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) production. Conclusion: ACT alleviates LOP-induced STC-like injury, and this protection is associated with attenuation of NLRP3 inflammasome activation and preservation of ENS integrity, while additional NLRP3-independent mechanisms may also contribute.
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