Natural Dietary Flavonoid Apigenin Mitigates Ulcerative Colitis via Modulating the AMPK/NF-κB/NLRP3 Signaling Axis

Area of Science:

• Natural product chemistry
• Gastroenterology
• Immunology

Background:

• Ulcerative colitis (UC) presents challenges with high relapse and low remission rates, necessitating novel complementary treatments.
• Apigenin (Api), a flavonoid found in parsley and celery, possesses known antioxidant and anti-inflammatory properties.
• Current therapeutic strategies for UC often require safer and more effective options.

Purpose of the Study:

• To investigate the therapeutic potential of apigenin (Api) as a complementary treatment for ulcerative colitis (UC).
• To elucidate the molecular mechanisms underlying apigenin's anti-inflammatory effects in a mouse model of colitis.

Main Methods:

• Acute colitis was induced in mice using 2.5% DSS.
• Apigenin (Api) was administered to assess its effects on disease severity, oxidative stress, and inflammation.
• Molecular mechanisms involving AMPK, NF-κB, and NLRP3 inflammasome activation were investigated.

Main Results:

• Apigenin administration significantly alleviated DSS-induced colitis symptoms, including weight loss, colon shortening, and disease activity index (DAI) scores.
• Api treatment restored mucosal integrity and reduced markers of oxidative stress and inflammation in the colon.
• Mechanistically, apigenin was found to directly activate AMPK and bind to NLRP3, suppressing the NF-κB pathway and NLRP3 inflammasome activation.

Conclusions:

• Apigenin demonstrates protective effects against colitis in mice through dual targeting of the AMPK/NF-κB/NLRP3 axis.
• Api cooperatively suppresses oxidative stress and inflammation, highlighting its potential as a natural anti-inflammatory agent for intestinal health.
• These findings support apigenin's potential as a safe and effective complementary therapeutic agent for ulcerative colitis.