Enhancing the efficacy of ulcerative colitis treatment by inhibiting LCN2-mediated pyroptosis through traditional processing techniques: With the rhizome of Atractylodes macrocephala Koidz. as an example.

What To Know

This paper compared raw Atractylodes macrocephala rhizome (AMR) with a rice-washed–processed form (R‑AMR) in a DSS mouse model of ulcerative colitis and in cell experiments. Both forms reduced disease activity, inflammation, and helped restore tight junction proteins; R‑AMR showed stronger effects.

The authors used bioinformatics, machine learning, and molecular docking to nominate Lipocalin‑2 (LCN2) and TIMP1 as targets and identified atractylenolide I (Atr I) as a likely active component binding LCN2.

In cell (LPS‑treated NCM460) and mouse experiments the study links therapeutic effects to inhibition of an LCN2 → NLRP3 → caspase‑1 → GSDMD pyroptosis pathway, with reduced IL‑1β/IL‑18/TNF‑α/IL‑6 and improved tight junction markers (ZO‑1, claudin‑1, MUC2). Knockdown of LCN2 lowered inflammasome activation and pyroptosis markers in vitro.

The work supports a mechanistic hypothesis that processing (rice‑washed water) alters AMR chemistry to increase Atr I activity against LCN2. The report is presented as an abstract/summary of experiments in mice and cells rather than a clinical trial. It does not provide human data or clinical dosing guidance, so it should not be taken as treatment advice.