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Article: Dexamethasone delays ulcer healing by inhibition of angiogenesis in rat stomachs

TitleDexamethasone delays ulcer healing by inhibition of angiogenesis in rat stomachs
Authors
KeywordsGastric ulcer
bFGF (basic fibroblast growth factor)
Angiogenesis
Dexamethasone
VEGF (vascular endothelial growth factor)
Prostaglandin E2
Issue Date2004
Citation
European Journal of Pharmacology, 2004, v. 485, n. 1-3, p. 275-281 How to Cite?
AbstractUsing the non-ulcerogenic doses of dexamethasone, we explored the action of glucocorticoids on ulcer healing and its relationship with angiogenic factors in the gastric mucosa. We applied dexamethasone (0.1 or 0.2 mg/kg/day) intragastrically in rats with acetic acid-induced gastric ulcer. The mucosal prostaglandin E2 level and protein expressions of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) at the ulcer margin were determined. Ulcer induction significantly increased protein expressions of bFGF, VEGF, and prostaglandin E2 level at the ulcer margin together with angiogenesis at the ulcer margin and base. The non-ulcerogenic doses of dexamethasone inhibited angiogenesis at the ulcer margin and ulcer base and delayed ulcer healing. These were associated with a significant decrease of prostaglandin E2 level and VEGF expression, but not the bFGF expression. Supplementation with prostaglandin E2 attenuated the inhibitory action of dexamethasone on VEGF expression and reversed the adverse effects of dexamethasone on angiogenesis and ulcer healing, without influencing bFGF expression. We concluded that dexamethasone given at non-ulcerogenic doses could decrease angiogenesis and delay acetic acid-induced ulcer healing; these actions were at least, in part, due to depletion of prostaglandin E2 level followed by down-regulation of VEGF at the ulcer margin of the stomach. © 2003 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/207501
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115

 

DC FieldValueLanguage
dc.contributor.authorLuo, Jiingchyuan-
dc.contributor.authorShin, Vivianyvonne-
dc.contributor.authorLiu, Edgar Shiu Lam-
dc.contributor.authorYe, Yini-
dc.contributor.authorWu, William Ka Kei-
dc.contributor.authorSo, Wallace Hau Leung-
dc.contributor.authorChang, Fullyoung-
dc.contributor.authorCho, Chihin-
dc.date.accessioned2014-12-31T01:01:47Z-
dc.date.available2014-12-31T01:01:47Z-
dc.date.issued2004-
dc.identifier.citationEuropean Journal of Pharmacology, 2004, v. 485, n. 1-3, p. 275-281-
dc.identifier.issn0014-2999-
dc.identifier.urihttp://hdl.handle.net/10722/207501-
dc.description.abstractUsing the non-ulcerogenic doses of dexamethasone, we explored the action of glucocorticoids on ulcer healing and its relationship with angiogenic factors in the gastric mucosa. We applied dexamethasone (0.1 or 0.2 mg/kg/day) intragastrically in rats with acetic acid-induced gastric ulcer. The mucosal prostaglandin E2 level and protein expressions of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) at the ulcer margin were determined. Ulcer induction significantly increased protein expressions of bFGF, VEGF, and prostaglandin E2 level at the ulcer margin together with angiogenesis at the ulcer margin and base. The non-ulcerogenic doses of dexamethasone inhibited angiogenesis at the ulcer margin and ulcer base and delayed ulcer healing. These were associated with a significant decrease of prostaglandin E2 level and VEGF expression, but not the bFGF expression. Supplementation with prostaglandin E2 attenuated the inhibitory action of dexamethasone on VEGF expression and reversed the adverse effects of dexamethasone on angiogenesis and ulcer healing, without influencing bFGF expression. We concluded that dexamethasone given at non-ulcerogenic doses could decrease angiogenesis and delay acetic acid-induced ulcer healing; these actions were at least, in part, due to depletion of prostaglandin E2 level followed by down-regulation of VEGF at the ulcer margin of the stomach. © 2003 Elsevier B.V. All rights reserved.-
dc.languageeng-
dc.relation.ispartofEuropean Journal of Pharmacology-
dc.subjectGastric ulcer-
dc.subjectbFGF (basic fibroblast growth factor)-
dc.subjectAngiogenesis-
dc.subjectDexamethasone-
dc.subjectVEGF (vascular endothelial growth factor)-
dc.subjectProstaglandin E2-
dc.titleDexamethasone delays ulcer healing by inhibition of angiogenesis in rat stomachs-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ejphar.2003.11.038-
dc.identifier.pmid14757151-
dc.identifier.scopuseid_2-s2.0-1642538365-
dc.identifier.volume485-
dc.identifier.issue1-3-
dc.identifier.spage275-
dc.identifier.epage281-

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