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Updated: May 23, 2025
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Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
Published on: January 5, 2017
12.2K
Apigenin ameliorates inflamed ulcerative colitis by regulating mast cell degranulation via the PAMP-MRGPRX2 feedback
Yihan Huang1, Na Wang2, Xiaolan Ji1
1School of Pharmacy, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China.
Summary
Apigenin (API) effectively treats ulcerative colitis (UC) by inhibiting mast cell degranulation and blocking inflammatory pathways. This natural flavonoid offers a promising therapeutic strategy for UC by targeting the PAMP-MRGPRX2 signaling axis.
Area of Science:
- Immunology
- Gastroenterology
- Pharmacology
Background:
- Ulcerative colitis (UC) progression is linked to a pro-inflammatory feedback loop involving Mas-related G-protein-coupled receptor X2 (MRGPRX2) and its ligand PAMP-12.
- Targeting MRGPRX2 for UC treatment remains underexplored, despite the anti-inflammatory potential of natural compounds like Apigenin (API).
Purpose of the Study:
- To investigate the therapeutic effect of Apigenin (API) on ulcerative colitis (UC).
- To elucidate the mechanism of API's action via the regulation of PAMP-MRGPRX2-mediated mast cell (MC) degranulation.
Main Methods:
- A dextran sodium sulfate (DSS)-induced mouse model of UC was employed.
- Evaluations included animal behavior, serological assays, histological analysis, mRNA sequencing, PCR, ELISA, and Western blotting in wild-type and MC MrgprB2-conditional knockout mice.
- In vitro and in vivo models of PAMP-12 triggered MC degranulation were used to study API's mechanism.
Main Results:
- Mast cell (MC) degranulation via MrgprB2 is critical for persistent colitis inflammation.
- API attenuated colonic tissue damage, splenomegaly, and myeloperoxidase activity, while improving crypt structure and reducing inflammatory cell infiltration.
- API suppressed MC degranulation and carboxypeptidases A3 (CPA3) levels, disrupting the PAMP-MrgprB2 pro-inflammatory feedback loop and inhibiting PAMP-12-triggered MC degranulation via Akt1/XBP-1S/CHOP/TXNIP and NF-κB/IL-1β pathways.
Conclusions:
- Apigenin (API) alleviates UC inflammatory symptoms.
- API acts by suppressing the PAMP-MRGPRX2/B2 mediated sustained MC degranulation feedback loop.
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