Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules

Ulcerative colitis (UC) is a serious health condition and defined as inflammation in the colon. Untreated, UC can develop into colitis-associated cancer (CAC), for which effective medicines are not available. Natural products are a better choice to treat UC by alleviating the inflammation. Caffeic a...

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Main Authors: Pandurangan, Ashok Kumar, Mohebali, Nooshin, Hasanpourghadi, Mohadeseh, Esa, Norhaizan Mohd
Format: Article
Published: Springer 2022
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Online Access:http://eprints.um.edu.my/33476/
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spelling my.um.eprints.334762022-08-04T01:42:30Z http://eprints.um.edu.my/33476/ Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules Pandurangan, Ashok Kumar Mohebali, Nooshin Hasanpourghadi, Mohadeseh Esa, Norhaizan Mohd QD Chemistry QH301 Biology QR Microbiology TP Chemical technology Ulcerative colitis (UC) is a serious health condition and defined as inflammation in the colon. Untreated, UC can develop into colitis-associated cancer (CAC), for which effective medicines are not available. Natural products are a better choice to treat UC by alleviating the inflammation. Caffeic acid phenethyl ester (CAPE) is a phenolic compound and known for its beneficial effects, including antibacterial, anti-inflammatory, anti-diabetic, and anticancer. We aimed to study the effect of CAPE on dextran sulfate sodium (DSS)-induced UC in mouse model. Administration of CAPE to DSS-induced mice protected against colon damage by improving body weight of mice, reducing the weight of spleen, and increased colon length. In addition, administration of CAPE resulted reduced the activity of myeloperoxidase (MPO) and CD68+ positive cells. Furthermore, a significant decrease in the production of key cytokines and the expression of nuclear factor (p65-NF)-kappa B. Moreover, p65-NF-kappa B activation was reduced in lipopolysaccharide (LPS)-treated RAW 264.7 macrophage cells from mouse origin. CAPE treatment leads to the reduced expressions of intercellular adhesion molecules (ICAM)- 1 and vascular cell adhesion molecules (VCAM), both are key cell adhesion molecules. The results of this study clearly indicate that CAPE can potentially control inflammation in the colon and can be used as a therapy for UC. Springer 2022-03 Article PeerReviewed Pandurangan, Ashok Kumar and Mohebali, Nooshin and Hasanpourghadi, Mohadeseh and Esa, Norhaizan Mohd (2022) Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules. Applied Biochemistry and Biotechnology, 194 (3, SI). pp. 1091-1104. ISSN 0273-2289, DOI https://doi.org/10.1007/s12010-021-03788-2 <https://doi.org/10.1007/s12010-021-03788-2>. 10.1007/s12010-021-03788-2
institution Universiti Malaya
building UM Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Malaya
content_source UM Research Repository
url_provider http://eprints.um.edu.my/
topic QD Chemistry
QH301 Biology
QR Microbiology
TP Chemical technology
spellingShingle QD Chemistry
QH301 Biology
QR Microbiology
TP Chemical technology
Pandurangan, Ashok Kumar
Mohebali, Nooshin
Hasanpourghadi, Mohadeseh
Esa, Norhaizan Mohd
Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules
description Ulcerative colitis (UC) is a serious health condition and defined as inflammation in the colon. Untreated, UC can develop into colitis-associated cancer (CAC), for which effective medicines are not available. Natural products are a better choice to treat UC by alleviating the inflammation. Caffeic acid phenethyl ester (CAPE) is a phenolic compound and known for its beneficial effects, including antibacterial, anti-inflammatory, anti-diabetic, and anticancer. We aimed to study the effect of CAPE on dextran sulfate sodium (DSS)-induced UC in mouse model. Administration of CAPE to DSS-induced mice protected against colon damage by improving body weight of mice, reducing the weight of spleen, and increased colon length. In addition, administration of CAPE resulted reduced the activity of myeloperoxidase (MPO) and CD68+ positive cells. Furthermore, a significant decrease in the production of key cytokines and the expression of nuclear factor (p65-NF)-kappa B. Moreover, p65-NF-kappa B activation was reduced in lipopolysaccharide (LPS)-treated RAW 264.7 macrophage cells from mouse origin. CAPE treatment leads to the reduced expressions of intercellular adhesion molecules (ICAM)- 1 and vascular cell adhesion molecules (VCAM), both are key cell adhesion molecules. The results of this study clearly indicate that CAPE can potentially control inflammation in the colon and can be used as a therapy for UC.
format Article
author Pandurangan, Ashok Kumar
Mohebali, Nooshin
Hasanpourghadi, Mohadeseh
Esa, Norhaizan Mohd
author_facet Pandurangan, Ashok Kumar
Mohebali, Nooshin
Hasanpourghadi, Mohadeseh
Esa, Norhaizan Mohd
author_sort Pandurangan, Ashok Kumar
title Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules
title_short Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules
title_full Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules
title_fullStr Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules
title_full_unstemmed Caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules
title_sort caffeic acid phenethyl ester attenuates dextran sulfate sodium-induced ulcerative colitis through modulation of nf-kappa b and cell adhesion molecules
publisher Springer
publishDate 2022
url http://eprints.um.edu.my/33476/
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score 13.211869