RESUMEN
BACKGROUND: Galli gigeriae endothelium corneum (GGEC) has been effectively used for centuries for the treatment of functional dyspepsia (FD) in clinical practice in Asian countries. However, its potential mechanism and chemical composition remains undertermined. METHODS: In this study, the chemical profile of GGEC ethyl acetate extract (EAE) was evaluated by HPLC-Q-TOF-MS/MS. The effects of EAE on intestinal barrier function and inflammation were investigated in IEC-6 cells and RAW264.7 cells. RESULTS: The results showed that 33 compounds were tentatively identified, including 12 soy isoflavones, 7 bile acids for the first time in EAE. EAE significantly reinforced intestinal barrier function via increasing the tight junction protein levels of ZO-1 and Occludin, reducing the mRNA expression levels of interleukin (IL)-1ß and IL-6 in tumor necrosis factor alpha (TNF-α)-challenged IEC-6 cells. The scratch wound assay showed that EAE accelerated wound healing of IEC-6 cells. EAE evidently reduced the level of NO in a dose-dependent manner with an IC50 value of 18.12 µg/mL, and the mRNA expression of TNF-α, IL-1ß, IL-6, iNOS and COX-2 in LPS-treated RAW264.7 cells. CONCLUSION: This study revealed the intestinal barrier protective effects and chemical profile of GGEC, and the results indicated that GGEC strengthened the intestinal barrier by up-regulating protein expression of tight junctions and limiting inflammatory responses.
RESUMEN
Managing patients with refractory inflammatory bowel diseases (IBD) is a common clinical challenge. Galli Gigeriae Endothelium Corneum (GGEC), a chicken by-product, has been used for centuries in Asian countries as a functional food and supplement for the treatment of gastrointestinal disorders. In this study, a novel peptide (LNLYP, LP-5) with gastrointestinal stability that can enhance the intestinal barrier function that was first identified in GGEC. Our work demonstrated that aryl hydrocarbon receptor (AhR) activation by LP-5 could inhibit the Src kinase to increase tight junction protein levels and down-regulate the expression of inflammatory cytokines to protect the intestinal barrier and finally alleviate dextran sulfate sodium (DSS)-induced colitis. This study revealed that LP-5 had the potential to develop into a therapeutic agent for the treatment of colitis and provided new high-valued utilization of GGEC.
