Publication: Ameliorative effects of riboflavin on acetic acid-induced colonic injury in rats
dc.contributor.author | ERTAŞ, BÜŞRA | |
dc.contributor.authors | Karakoyun, Berna; Ertas, Busra; Yuksel, Meral; Akakin, Dilek; Cevik, Ozge; Sener, Goksel | |
dc.date.accessioned | 2022-03-12T22:26:00Z | |
dc.date.available | 2022-03-12T22:26:00Z | |
dc.date.issued | 2018 | |
dc.description.abstract | Riboflavin (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.doi | 10.1111/1440-1681.12894 | |
dc.identifier.issn | 1440-1681 | |
dc.identifier.pubmed | 29164668 | |
dc.identifier.uri | https://hdl.handle.net/11424/235000 | |
dc.identifier.wos | WOS:000433569300009 | |
dc.language.iso | eng | |
dc.publisher | WILEY | |
dc.relation.ispartof | CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject | acetic acid | |
dc.subject | colitis | |
dc.subject | oxidative damage | |
dc.subject | riboflavin | |
dc.subject | INFLAMMATORY-BOWEL-DISEASE | |
dc.subject | ULCERATIVE-COLITIS | |
dc.subject | DNA-DAMAGE | |
dc.subject | OXIDATIVE STRESS | |
dc.subject | TNF-ALPHA | |
dc.subject | GROWTH | |
dc.subject | BETA | |
dc.subject | ACTIVATION | |
dc.subject | EXPRESSION | |
dc.subject | CELLS | |
dc.title | Ameliorative effects of riboflavin on acetic acid-induced colonic injury in rats | |
dc.type | article | |
dspace.entity.type | Publication | |
local.avesis.id | f94b9dcc-9fc2-431d-a58b-fe27aa0485c2 | |
local.import.package | SS17 | |
local.indexed.at | WOS | |
local.indexed.at | SCOPUS | |
local.indexed.at | PUBMED | |
local.journal.numberofpages | 10 | |
local.journal.quartile | Q3 | |
oaire.citation.endPage | 572 | |
oaire.citation.issue | 6 | |
oaire.citation.startPage | 563 | |
oaire.citation.title | CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY | |
oaire.citation.volume | 45 | |
relation.isAuthorOfPublication | 864e7cb0-b39f-48bb-a546-ee65ffc807b2 | |
relation.isAuthorOfPublication.latestForDiscovery | 864e7cb0-b39f-48bb-a546-ee65ffc807b2 |