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Article: Association of Heparin with Basic Fibroblast Growth Factor, Epidermal Growth Factor, and Constitutive Nitric Oxide Synthase on Healing of Gastric Ulcer in Rats

TitleAssociation of Heparin with Basic Fibroblast Growth Factor, Epidermal Growth Factor, and Constitutive Nitric Oxide Synthase on Healing of Gastric Ulcer in Rats
Authors
Issue Date1999
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org/
Citation
The Journal of Pharmacology and Experimental Therapeutics, 1999, v. 290 n. 2, p. 789-796 How to Cite?
AbstractThe healing effect of heparin on gastric ulcer and its underlying mechanisms were studied. The influences of protamine on these effects were also investigated. Gastric ulcer was induced by acetic acid in rats. Heparin (100-1000 U/kg i.v.) was given once daily for 4 or 7 days. Ulcer area was measured; gastric mucosal regeneration, proliferation, and angiogenesis were determined by histological or immunohistochemical methods. Gastric mucosal basic fibroblast growth factor (bFGF) level was assessed by an enzyme-linked immunosorbent assay, and the mucosal epidermal growth factor (EGF) level and nitric oxide synthase (NOS) activity were measured by radioimmunoassay. The anticoagulant action of heparin was determined by the duration of bleeding time. The results showed that heparin given for 4 or 7 days significantly accelerated gastric ulcer healing in a dose-dependent manner. The three doses of heparin significantly stimulated mucosal regeneration and proliferation as well as angiogenesis but not the contraction of ulcer base. Similar effects were observed in gastric mucosal bFGF and EGF levels and constitutive NOS activity. Protamine not only abolished the anticoagulant action of heparin but also significantly potentiated its effects on ulcer healing, gastric mucosal proliferation, angiogenesis, and constitutive NOS activity. These findings indicate that heparin can accelerate gastric ulcer healing, which is associated with mucosal regeneration, proliferation, and angiogenesis. These actions are likely to be stimulated by bFGF, EGF, and constitutive NOS activity in the gastric mucosa. Protamine potentiates the ulcer-healing effect of heparin, which is probably acting through constitutive NOS activation.
Persistent Identifierhttp://hdl.handle.net/10722/211451
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847

 

DC FieldValueLanguage
dc.contributor.authorLi, Y-
dc.contributor.authorWang, HY-
dc.contributor.authorCho, CH-
dc.date.accessioned2015-07-14T04:10:32Z-
dc.date.available2015-07-14T04:10:32Z-
dc.date.issued1999-
dc.identifier.citationThe Journal of Pharmacology and Experimental Therapeutics, 1999, v. 290 n. 2, p. 789-796-
dc.identifier.issn0022-3565-
dc.identifier.urihttp://hdl.handle.net/10722/211451-
dc.description.abstractThe healing effect of heparin on gastric ulcer and its underlying mechanisms were studied. The influences of protamine on these effects were also investigated. Gastric ulcer was induced by acetic acid in rats. Heparin (100-1000 U/kg i.v.) was given once daily for 4 or 7 days. Ulcer area was measured; gastric mucosal regeneration, proliferation, and angiogenesis were determined by histological or immunohistochemical methods. Gastric mucosal basic fibroblast growth factor (bFGF) level was assessed by an enzyme-linked immunosorbent assay, and the mucosal epidermal growth factor (EGF) level and nitric oxide synthase (NOS) activity were measured by radioimmunoassay. The anticoagulant action of heparin was determined by the duration of bleeding time. The results showed that heparin given for 4 or 7 days significantly accelerated gastric ulcer healing in a dose-dependent manner. The three doses of heparin significantly stimulated mucosal regeneration and proliferation as well as angiogenesis but not the contraction of ulcer base. Similar effects were observed in gastric mucosal bFGF and EGF levels and constitutive NOS activity. Protamine not only abolished the anticoagulant action of heparin but also significantly potentiated its effects on ulcer healing, gastric mucosal proliferation, angiogenesis, and constitutive NOS activity. These findings indicate that heparin can accelerate gastric ulcer healing, which is associated with mucosal regeneration, proliferation, and angiogenesis. These actions are likely to be stimulated by bFGF, EGF, and constitutive NOS activity in the gastric mucosa. Protamine potentiates the ulcer-healing effect of heparin, which is probably acting through constitutive NOS activation.-
dc.languageeng-
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org/-
dc.relation.ispartofThe Journal of Pharmacology and Experimental Therapeutics-
dc.subject.meshAnti-Ulcer Agents - therapeutic use-
dc.subject.meshAnticoagulants - therapeutic use-
dc.subject.meshEpidermal Growth Factor - metabolism - physiology-
dc.subject.meshFibroblast Growth Factor 2 - metabolism - physiology-
dc.subject.meshHeparin - therapeutic use-
dc.titleAssociation of Heparin with Basic Fibroblast Growth Factor, Epidermal Growth Factor, and Constitutive Nitric Oxide Synthase on Healing of Gastric Ulcer in Rats-
dc.typeArticle-
dc.identifier.emailCho, CH: chcho@hkusua.hku.hk-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.pmid10411593-
dc.identifier.hkuros45656-
dc.identifier.volume290-
dc.identifier.issue2-
dc.identifier.spage789-
dc.identifier.epage796-
dc.publisher.placeUnited States-

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