期刊
FRONTIERS IN NUTRITION
卷 8, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fnut.2021.723480
关键词
beta-carotene; colonic inflammation; colonic epithelial cells; tight junctions; vitamin A
资金
- USDA National Institute of Food and Agriculture [1021933]
- National Science Foundation [1643814]
- Direct For Education and Human Resources
- Division Of Undergraduate Education [1643814] Funding Source: National Science Foundation
The study found that beta-carotene can alleviate colonic inflammation and enhance tight junction proteins levels in an in vitro epithelial cell model, potentially improving barrier function.
Background: Carotenoids are naturally occurring pigments accounting for the brilliant colors of fruits and vegetables. They may display antioxidant and anti-inflammatory properties in humans besides being precursors to vitamin A. There is a gap of knowledge in examining their role within colonic epithelial cells. We proposed to address this research gap by examining the effects of a major dietary carotenoid, beta-carotene, in the in vitro epithelial cell model. Methods: We examined the function of beta-carotene in the lipopolysaccharide (LPS)/toll-like receptor 4 (TLR4) signaling pathway. We conducted western blotting assays to evaluate expressions of TLR4 and its co-receptor, CD14. We also examined NF-kappa B p65 subunit protein levels in the model system. Furthermore, we studied the impact of beta-carotene on the tight junction proteins, claudin-1, and occludin. We further carried out immunocytochemistry experiments to detect and visualize claudin-1 expression. Results: beta-Carotene reduced LPS-induced intestinal inflammation in colonic epithelial cells. beta-Carotene also promoted the levels of tight junction proteins, which might lead to enhanced barrier function. Conclusions: beta-Carotene could play a role in modulating the LPS-induced TLR4 signaling pathway and in enhancing tight junction proteins. The findings will shed light on the role of beta-carotene in colonic inflammation and also potentially in metabolic disorders since higher levels of LPS might induce features of metabolic diseases.
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