Qingqiao polyphenols improve DSS induced ulcerative colitis in mice by inhibiting NLRP3/AIM2 inflammasome mediated pyroptosis

Bibliographic Data

ID21543993
AuthorsLimin Chao (Henan Institute of Science and Technology), Wenjing Zhang (0000-0002-1810-791X, Henan Institute of Science and Technology), Yuchao Feng (Henan Institute of Science and Technology), Wen Li (0009-0001-7707-3780, Henan Institute of Science and Technology), Yang Liang (0000-0002-4226-9580, Henan Institute of Science and Technology), Yangming Liang, Pei Gao (0000-0003-2061-0861, Henan Institute of Science and Technology), Li Wang (0000-0002-3460-2080), Yan Li (0000-0001-6650-7726, Henan Institute of Science and Technology), Jinyou Ma (Henan Institute of Science and Technology), Yan Yu (0000-0003-4031-252X, Henan Institute of Science and Technology, corresponding author)
Year2026
Volume354
Pages120480
Publication date2026-01-01
Open AccessYes
TypeARTICLE
VenueJournal of Ethnopharmacology (JOURNAL)
Journal identifiersISSN: 0378-8741 • E-ISSN: 1872-7573
PublisherElsevier BV (PUBLISHER)
DOI10.1016/j.jep.2025.120480
PMID40876794
OpenAlexW4413845325
LanguageEN
References cited39

ETHNOPHARMACOLOGICAL RELEVANCE: Qingqiao is a traditional Chinese medicine widely used for its heat-clearing, detoxifying, antibacterial, and anti-inflammatory properties. Due to these therapeutic effects, it has been commonly employed in the treatment of intestinal inflammatory disorders in China. AIMS OF THIS STUDY: This study aimed to investigate the therapeutic effects of Qingqiao polyphenols (QP) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) and elucidate the underlying mechanisms, particularly the roles of NLRP3 and AIM2 inflammasomes in regulating pyroptosis. METHODS: Using a DSS-induced murine UC model and an in vitro pyroptosis model in J774A.1 macrophages, we evaluated the protective effects of QP and explored its mechanisms of action. RESULTS: QP can significantly reduce the levels of inflammatory factors and oxidative stress in UC mice. Further investigation revealed that QP improve UC symptoms by inhibiting the NLRP3/AIM2 inflammasomes and pyroptosis. Consistent results were observed in in vitro experiments, where QP reduced lactate dehydrogenase (LDH) levels and pyroptosis occurrence in J774A.1 cells. Intriguingly, upon NLRP3 inhibition, we observed a compensatory upregulation of AIM2, accompanied by increased levels of GSDMD, IL-1β, and LDH release, suggesting that AIM2 may drive pyroptosis in the absence of NLRP3. Furthermore, AIM2 overexpression led to elevated GSDMD and IL-1β while significantly downregulating NLRP3 expression, indicating a competitive interaction between NLRP3 and AIM2 in pyroptotic signaling. CONCLUSIONS: We found that QP improve DSS-induced UC by inhibiting NLRP3/AIM2 inflammasome-mediated pyroptosis. Moreover, we uncovered a dynamic crosstalk between NLRP3 and AIM2, where compensatory mechanisms may sustain pyroptosis when one pathway is suppressed.

AIM2 · Antioxidant · Biology · Caspase 1 · Colitis · Disease · Inflammasome · Inflammation · Polyphenol · Pyroptosis · Ulcerative colitis · Autoimmune and Inflammatory Disorders Research · Biochemistry · Calcium signaling and nucleotide metabolism · Chemistry · IL-33, ST2, and ILC Pathways · Immunology · Inflammasome and immune disorders · Inflammation biomarkers and pathways · Internal Medicine · Medicine · Pharmacology

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