Antioxidant and anti-inflammatory effects of hesperidin methyl chalcone in experimental ulcerative colitis

Neutrophil infiltration, pro-inflammatory cytokines, and reactive oxygen species (ROS) production have been implicated in development and progression of ulcerative colitis (UC), an inflammatory bowel disease (IBD) characterized by ulcerating inflammation of the mucosal layer generally restricted to...

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Veröffentlicht in:Chemico-biological interactions 2021-01, Vol.333, p.109315-109315, Article 109315
Hauptverfasser: Guazelli, Carla F.S., Fattori, Victor, Ferraz, Camila R., Borghi, Sergio M., Casagrande, Rubia, Baracat, Marcela M., Verri, Waldiceu A.
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container_title Chemico-biological interactions
container_volume 333
creator Guazelli, Carla F.S.
Fattori, Victor
Ferraz, Camila R.
Borghi, Sergio M.
Casagrande, Rubia
Baracat, Marcela M.
Verri, Waldiceu A.
description Neutrophil infiltration, pro-inflammatory cytokines, and reactive oxygen species (ROS) production have been implicated in development and progression of ulcerative colitis (UC), an inflammatory bowel disease (IBD) characterized by ulcerating inflammation of the mucosal layer generally restricted to the colon. The side effects, safety and human intolerance are limitations of the currently approved treatments for UC. Hesperidin methyl chalcone (HMC) is a flavonoid used to treat chronic venous disease, which shows anti-inflammatory, analgesic, and antioxidant properties in pre-clinical studies, however, its effects on colitis have never been described. Therefore, we aimed to evaluate the protective effects of HMC in a mouse model of acetic acid-induced colitis. Treatment with HMC significantly reduced neutrophil infiltration, edema, colon shortening, macro and microscopic damages induced by intracolonic administration of acetic acid. The improvement of colitis after HMC treatment is related to the increase in colon antioxidant status, and the inhibition of pro-inflammatory cytokines TNF-α, IL-6, IL-1β, and IL-33 in the colon. We observed, moreover, that HMC inhibited NF-κB activation in the colon, which might explain the reduction of the cytokines we observed. Finally, these results demonstrate a novel applicability of HMC to increase antioxidant response and reduce inflammation during acetic acid-induced colitis suggesting it as a promising therapeutic approach for the treatment of ulcerative colitis. •Methylation of hesperidin produces hesperidin methyl chalcone (HMC).•HMC inhibited neutrophil infiltration, edema and colon shortening in mouse colitis.•HMC also inhibited macroscopic and microscopic damages in colitis.•HMC reduced oxidative stress, cytokine production and NF-κB activation.•This is the first study demonstrating that HMC treats experimental ulcerative colitis.
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subjects Animals
Anti-Inflammatory Agents - pharmacology
Anti-Inflammatory Agents - therapeutic use
Antioxidants - pharmacology
Antioxidants - therapeutic use
Chalcones - pharmacology
Chalcones - therapeutic use
Colitis, Ulcerative - complications
Colitis, Ulcerative - drug therapy
Colitis, Ulcerative - immunology
Colitis, Ulcerative - metabolism
Colon - drug effects
Colon - pathology
Cytokines - biosynthesis
Disease Models, Animal
Edema - complications
Hesperidin - analogs & derivatives
Hesperidin - pharmacology
Hesperidin - therapeutic use
Hesperidin methyl chalcone
Inflammation
Male
Mice
Neutrophil Infiltration - drug effects
NF-kappa B - metabolism
Oxidative stress
Oxidative Stress - drug effects
Ulcerative colitis
title Antioxidant and anti-inflammatory effects of hesperidin methyl chalcone in experimental ulcerative colitis
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