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Atractylodide I

Preliminary

Mechanism of Action

Inhibits NF-κB signaling by preventing IκBα phosphorylation and subsequent p65 nuclear translocation, suppressing transcription of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. Modulates Toll-like receptor 4 (TLR4) downstream signaling cascades including MyD88-dependent and TRIF-dependent pathways, reducing macrophage hyperactivation. Also demonstrates NLRP3 inflammasome inhibitory activity and upregulates mucosal epidermal growth factor (EGF) receptor expression, contributing to gastroprotective and wound-healing effects in the gastrointestinal epithelium.

Research Notes

In vitro studies using LPS-stimulated RAW264.7 macrophage models demonstrate dose-dependent anti-inflammatory effects of atractylodide I, with IC50 values for TNF-α suppression in the low micromolar range. Rodent studies in colitis (DSS-induced) and sepsis (cecal ligation and puncture) models have confirmed significant reduction in systemic inflammatory markers and improved mucosal integrity scores. A 2019 study in Journal of Ethnopharmacology documented specific gastroprotective effects via EGF receptor upregulation and mucosal glycoprotein restoration, supporting the traditional application of Bai Zhu in digestive disorders.

Found In 1 Herb

3D Molecular Structure

Sesquiterpene lactone
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Atractylodide I

Sesquiterpene lactoneAromatic plant metabolites with anti-inflammatory properties

Representative pattern: C₂₁H₃₀O₂

Atoms
Carbon
Oxygen

Related Compounds (Sesquiterpene lactone)

Live Research

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These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. This content is for educational purposes only and is not a substitute for professional medical advice.