ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Atractylenolide III as a novel therapeutic strategy for gastric ulcer: mechanistic insights and investigation of molecular targets.
Article in Naunyn-Schmiedeberg's archives of 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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10 authors.
Funding
Abstract
purposeAtractylenolide III (AT-III) exhibits notable anti-inflammatory, neuroprotective, and gastroprotective properties; however, its protective mechanisms in the gastric mucosa remain unclear. This study aimed to investigate the protective effects and mechanism of action of AT-III against indomethacin (IND)-induced gastric mucosal injury in rats.
methodsNetwork pharmacological approaches were used to predict the therapeutic potential and underlying mechanisms of AT-III in gastric ulcers (GU). Gastric mucosal morphology and ultrastructure were assessed using hematoxylin and eosin (HE) staining, periodic acid-Schiff (PAS) staining, scanning electron microscopy (SEM), and transmission electron microscopy (TEM). Molecular docking was used to predict the binding affinity of AT-III with key molecular targets in the mitogen-activated protein kinase (MAPK)/nuclear factor-κB (NF-κB) signaling pathway. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunofluorescence assays were employed to detect the expression levels of Raf, MEK1/2, ERK1, IκBβ, IKKβ, and NF-κB in rat gastric tissues to verify the effects of AT-III on IND-induced GU and MAPK/NF-κB-mediated inflammatory responses.
resultsHistological and ultrastructural analyses revealed significant improvements in rat gastric mucosa following AT-III treatment. Molecular docking indicated strong binding affinity of AT-III to MAPK/NF-κB pathway targets. Subsequent qRT-PCR and immunofluorescence experiments confirmed these findings, demonstrating that AT-III downregulated mRNA and protein expressions of Raf, MEK1/2, ERK1, IκBβ, IKKβ, and NF-κB in rats.
conclusionBy inhibiting pivotal regulators within the MAPK/NF-κB signaling cascade, AT-III effectively reduced local inflammation, ameliorated the pathological morphology of IND-induced GU in rats, and enhanced therapeutic outcomes, indicating its potential as a therapeutic agent for GU.
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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.