Publication: Preventive effects of quercetin on the leaky gut by suppression of IL-1beta-induced transcription factors involved in an inflammatory pathway in colonic epithelial cells
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Issued Date
2023-10-01
Resource Type
ISSN
01256491
Scopus ID
2-s2.0-85197765724
Journal Title
Thai Journal of Veterinary Medicine
Volume
53
Issue
4
Start Page
459
End Page
470
Rights Holder(s)
SCOPUS
Bibliographic Citation
Thai Journal of Veterinary Medicine Vol.53 No.4 (2023) , 459-470
Suggested Citation
Chayalak W., Thammacharoen S., Deachapunya C., Poonyachoti S. Preventive effects of quercetin on the leaky gut by suppression of IL-1beta-induced transcription factors involved in an inflammatory pathway in colonic epithelial cells. Thai Journal of Veterinary Medicine Vol.53 No.4 (2023) , 459-470. 470. Retrieved from: https://hdl.handle.net/20.500.14740/20278
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Abstract
Flavonol quercetin (Q), found in vegetables and fruits, demonstrates the most potent anti-inflammatory effect. The preventive effect and cellular mechanisms of Q (Q1, Q10, and Q100 μM) on IL-1β induced leaky gut via the signaling molecules of inflammatory pathway, NF-κB p65-iκB/or p38/ERK1/2/MLCK/phospho(p)-MLC were investigated in Caco-2 cells. The cytotoxic effect of Q was initially determined by MTT assay. Transepithelial electrical resistance (TER) and apical-to-basolateral fluorescein isothiocyanate-labeled dextran (FD-4) flux were used to determine paracellular permeability. The protein expression of signaling molecules was examined by Western blot analysis, and their target MLCK mRNA expression was determined using real-time PCR. All Q treatments during 0 - 48 h with or without IL-1β (10 ng/ml) were not toxic and had no effect on TER except for a decrease in TER by Q100 at 24 h. Q1 and Q10 prevented IL-1β-induced increase in FD-4 flux associated with the inhibition of the MLCK gene transcription induced by IL-1β at 6 h after treatment. The inhibition of Q on the NF-κB p65, ERK1/2, MLCK, and p-MLC expression induced by IL-1β after 12 h and 24 h coincided. The results suggest the potential role of Q in manipulating the main therapeutic targets of intestinal barrier disruption.