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Collagen ultrastructure and TGF-beta 1 expression preserved with aminoguanidine during wound healing in diabetic rats

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dc.contributor.authorYAVUZ, DİLEK
dc.contributor.authorsYavuz, D; Tugtepe, H; Cetinel, S; Uyar, S; Kaya, H; Haklar, G; Civelek, S; Deyneli, O; San, T; Burcak, G; Akalin, S
dc.date.accessioned2022-03-12T15:59:27Z
dc.date.available2022-03-12T15:59:27Z
dc.date.issued2005
dc.description.abstractAdvanced glycoxidation end products have been implicated in delayed diabetic wound healing. In this study, we evaluated the effects of aminoguanidine, which is an advanced glycation and nitric oxide ( NO) synthase inhibitor, on extracellular matrix protein expression, collagen configuration, and nitrite/nitrate levels in wounds of diabetic rats. Sixteen Wistar male rats were made diabetic by streptozotocin. Of these, eight rats were given AG ( aminoguanidine bicarbonate ( AG) ( group DAG) in their drinking water, and eight rats were followed as diabetic paired controls ( group D). Eight healthy rats were followed as the healthy control group ( group H). At the eighth week, a 2 x 2 cm area full-thickness skin defect was created. The degree of contraction of the open wounds was evaluated for 2 weeks duration. On the 15th postoperative day, wound surface areas were measured, and wound specimens and blood samples were collected. The shrinking percentage of the wounds was small in both groups H and DAG compared with group D ( p < 0.05). Similar to healthy rats, the aminoguanidine-treated diabetic rats had very strong transforming growth factor ( TGF)-beta 1 expression in granulation tissue and intact skin in comparison with diabetic controls. In the diabetic group, the intact skin demonstrated sparsely distributed regular collagen fibers in the granulation zone, and the regular pattern of collagen fibers was lost. In conclusion, aminoguanidine improves wound healing, restores growth factor TGF-beta 1 expression, and preserves collagen ultra structure, whereas it has no prominent effect on NO levels within wound tissue in diabetic rats.
dc.identifier.doi10.1080/07435800500373140
dc.identifier.eissn1532-4206
dc.identifier.issn0743-5800
dc.identifier.pubmed16392625
dc.identifier.urihttps://hdl.handle.net/11424/224411
dc.identifier.wosWOS:000233635100008
dc.language.isoeng
dc.publisherTAYLOR & FRANCIS INC
dc.relation.ispartofENDOCRINE RESEARCH
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectadvanced glycation end products
dc.subjectaminoguanidine
dc.subjectwound healing
dc.subjectTGF-beta
dc.subjectdermal collagen
dc.subjectnitric oxide
dc.subjectlipid peroxidation
dc.subjectstreptozotocin-induced diabetes
dc.subjectENDOTHELIAL GROWTH-FACTOR
dc.subjectNITRIC-OXIDE SYNTHESIS
dc.subjectLIPID-PEROXIDATION
dc.subjectEND-PRODUCTS
dc.subjectNONENZYMATIC GLYCOSYLATION
dc.subjectINHIBITION
dc.subjectGLYCATION
dc.subjectMOUSE
dc.subjectMICE
dc.subjectCOMPLICATIONS
dc.titleCollagen ultrastructure and TGF-beta 1 expression preserved with aminoguanidine during wound healing in diabetic rats
dc.typeconferenceObject
dspace.entity.typePublication
local.avesis.id4a0df8b6-eab6-4337-9fe9-463838b4b527
local.conference.dateJUN 14-18, 2002
local.conference.locationSAN FRANCISCO, CA
local.conference.sponsorAmer Diabet Assoc
local.conference.title62nd Annual Meeting of the American-Diabetes-Association
local.import.packageSS15
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages15
oaire.citation.endPage243
oaire.citation.issue3
oaire.citation.startPage229
oaire.citation.titleENDOCRINE RESEARCH
oaire.citation.volume31
relation.isAuthorOfPublication26174ec5-7dca-4038-a7fe-9a43f236fd15
relation.isAuthorOfPublication.latestForDiscovery26174ec5-7dca-4038-a7fe-9a43f236fd15

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