Publication:
Ameliorative effects of riboflavin on acetic acid-induced colonic injury in rats

dc.contributor.authorERTAŞ, BÜŞRA
dc.contributor.authorsKarakoyun, Berna; Ertas, Busra; Yuksel, Meral; Akakin, Dilek; Cevik, Ozge; Sener, Goksel
dc.date.accessioned2022-03-12T22:26:00Z
dc.date.available2022-03-12T22:26:00Z
dc.date.issued2018
dc.description.abstractRiboflavin (RF) has been found to be a promising antioxidant and/or anti-inflammatory agent in several studies. However, the effect of RF against acetic acid (AA)-induced colonic injury is currently unknown. This study aimed to investigate the potential antioxidant and protective effects of RF in a rat model of ulcerative colitis. Starting immediately after the colitis induction (AA+RF group) or 1week before the colitis induction (RF+AA+RF group), the rats were treated with RF (25mg/kg per day; p.o.) for 3days. The control and AA groups received saline (1mL; p.o.) whereas AA+SS group (positive control) received sulfasalazine (100mg/kg per day; p.o.) for 3days. Colonic samples were taken for the biochemical and histological assessments on the third day. High damage scores, elevated tissue wet weight index (WI), tissue myeloperoxidase (MPO) activity, 8-hydroxy-2-deoxyguanosine levels and chemiluminescence values, and a pronounced decrease in antioxidant glutathione (GSH) levels of the AA group were all reversed by RF pretreatment (RF+AA+RF group) and SS treatment (AA+SS group) (P<.05-.001). Tissue WI, MPO activity and GSH levels were not statistically changed in the AA+RF group. Western blot analysis revealed that the decreased protein expressions of tissue collagen (COL) 1A1, COL3A1 and transforming growth factor-1 in the AA group were elevated in all the treatment groups (P<.05-.001). In conclusion, RF exerts both the antioxidant and anti-inflammatory effects against AA-induced colonic inflammation by suppressing neutrophil accumulation, inhibiting reactive oxidant generation, preserving endogenous glutathione, improving oxidative DNA damage and regulating inflammatory mediators, suggesting a future potential role in the treatment and prevention of ulcerative colitis.
dc.identifier.doi10.1111/1440-1681.12894
dc.identifier.issn1440-1681
dc.identifier.pubmed29164668
dc.identifier.urihttps://hdl.handle.net/11424/235000
dc.identifier.wosWOS:000433569300009
dc.language.isoeng
dc.publisherWILEY
dc.relation.ispartofCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectacetic acid
dc.subjectcolitis
dc.subjectoxidative damage
dc.subjectriboflavin
dc.subjectINFLAMMATORY-BOWEL-DISEASE
dc.subjectULCERATIVE-COLITIS
dc.subjectDNA-DAMAGE
dc.subjectOXIDATIVE STRESS
dc.subjectTNF-ALPHA
dc.subjectGROWTH
dc.subjectBETA
dc.subjectACTIVATION
dc.subjectEXPRESSION
dc.subjectCELLS
dc.titleAmeliorative effects of riboflavin on acetic acid-induced colonic injury in rats
dc.typearticle
dspace.entity.typePublication
local.avesis.idf94b9dcc-9fc2-431d-a58b-fe27aa0485c2
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages10
local.journal.quartileQ3
oaire.citation.endPage572
oaire.citation.issue6
oaire.citation.startPage563
oaire.citation.titleCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
oaire.citation.volume45
relation.isAuthorOfPublication864e7cb0-b39f-48bb-a546-ee65ffc807b2
relation.isAuthorOfPublication.latestForDiscovery864e7cb0-b39f-48bb-a546-ee65ffc807b2

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