Cucurbitacin B alleviates DSS-induced experimental colitis by targeting ZNF70 to suppress the NLRP3/STAT3 signaling

Shen Cao1, Yuhan Wang2, Yi Tai1

  • 1Molecular Medicine Research Center, College of Pharmacy, Ministry of Education Key Laboratory of Changbai Mountain Natural Resources and Functional Molecules), Yanbian University, Yanji, 133002, Jilin Province, China.

Inflammopharmacology
|August 12, 2025
PubMed

Insights

Cucurbitacin B (CuB) effectively reduces inflammation in ulcerative colitis (UC) models by regulating the NLRP3 inflammasome and p-STAT3 pathways. This natural compound offers potential for new UC treatments.

Area of Science:

  • Pharmacology
  • Immunology
  • Gastroenterology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease with complex pathogenesis.
  • Current UC treatments have limitations, necessitating novel therapeutic strategies.
  • Cucurbitacin B (CuB), a natural triterpenoid, possesses known anti-inflammatory properties.

Purpose of the Study:

  • To evaluate the anti-inflammatory efficacy of Cucurbitacin B (CuB) in experimental models of ulcerative colitis.
  • To elucidate the molecular mechanisms underlying CuB's anti-inflammatory effects.

Main Methods:

  • In vivo assessment using DSS-induced experimental colitis in mice.
  • In vitro studies utilizing macrophage models.
  • Analysis of NLRP3 inflammasome assembly and p-STAT3 activation.
  • Quantification of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α).

Main Results:

  • CuB demonstrated significant anti-inflammatory effects in both in vivo and in vitro models.
  • CuB regulated NLRP3 inflammasome assembly and p-STAT3 activation via ZNF70.
  • CuB reduced the release of key pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α.

Conclusions:

  • Cucurbitacin B exhibits potent anti-inflammatory activity relevant to ulcerative colitis management.
  • CuB's mechanism involves modulation of the NLRP3 inflammasome and STAT3 signaling pathways.
  • CuB presents a promising therapeutic candidate for preventing UC development and progression.

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