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Allomyrina dichotoma larval extract attenuates intestinal barrier disruption by altering inflammatory response and tight junction proteins in lipopolysaccharide-induced Caco-2 cells

Authors
Kim, K.Bae, G.-D.Park, E.-Y.Baek, D.J.Kim, C.Y.Jang, S.-E.Oh, Y.S.
Issue Date
Oct-2020
Publisher
Elsevier B.V.
Keywords
Allomyrina dichotoma larvae; Caco-2 cell; Inflammation; Intestinal permeability; Tight junction protein
Citation
Biochemical and Biophysical Research Communications, v.532, no.1, pp.145 - 150
Journal Title
Biochemical and Biophysical Research Communications
Volume
532
Number
1
Start Page
145
End Page
150
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/78749
DOI
10.1016/j.bbrc.2020.08.034
ISSN
0006-291X
Abstract
Intestinal epithelial cells form a barrier between the intestinal lumen and host connective tissues and play an important role in maintaining intestinal nutrient homeostasis. This study investigated effects of Allomyrina dichotoma (rhinoceros beetle) larval extract (ADLE) on the intestinal barrier damage and explored mechanisms for reversing intestinal barrier dysfunction in lipopolysaccharide (LPS)-stimulated Caco-2, human intestinal epithelial cells. LPS reduced intestinal epithelial barrier function by increasing transepithelial electrical resistance, and this effect was significantly attenuated by ADLE treatment. ADLE also significantly countered the inhibition of tight junction-related protein expression in both LPS-induced Caco-2 cells and intestine from HFD-induced mice. Moreover, ADLE significantly decreased expression and production of inflammatory factors, such as iNOS, cox-2, nitric oxide, and cytokines induced by LPS stimulus. Reduction in phosphorylation of adenosine monophosphate-activated protein kinase was averted by ADLE treatment in LPS treated INS-1 cells. Finally, reactive oxygen stress level was decreased and ATP production was increased by ADLE treatment. ADLE appears to display gut health-promoting effects by reducing inflammation and inducing tight junction proteins in Caco-2 cells. Therefore, ADLE might be useful for preventing or treating intestine cell damage in inflammatory bowel disease. © 2020 The Authors
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