A Novel Mechanism of Anti-T-Lymphocyte Globulin Mediated by Fractalkine in Renal Ischemia-Reperfusion Injury in Rats

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dc.contributor.authorGunay, Y.
dc.contributor.authorInal, A.
dc.contributor.authorYener, N.
dc.contributor.authorSinanoglu, O.
dc.contributor.authorSelvi, O.
dc.contributor.authorBircan, H. Y.
dc.date.accessioned2024-07-12T21:53:34Z
dc.date.available2024-07-12T21:53:34Z
dc.date.issued2013en_US
dc.departmentMaltepe Üniversitesien_US
dc.description.abstractBackground. Ischemia-reperfusion injury (IRI) is among the main challenges in kidney transplantation. It causes delayed graft function and graft loss in long-term follow-up studies. Anti-T lymphocyte globulin (ATG), a common induction immunosuppressive, has been used in kidney transplantation to prevent rejection. Fractalkine (FKN) is among the main chemokines involved in IRI. This study was designed to identify the relationship between ATG and FKN after warm ischemia in rat kidneys. Methods. Rats were divided into three groups: Control, IRI+normal saline(NS) and IRI+ATG. After IRI was initiated, rats received a dose of ATG or NS during surgery as well as two more doses at 24 and 48 hours after surgery. All rats were humanely killed at 72 hours. Results. The concentration of FKN as well as dendritic cells (DC) and macrophages were lower in both peripheral blood and the injured kidney among ATG-treated versus control rats. Additionally cell necrosis, cytoplasmic vacuolization, cast formation, and tubular dilatation were improved among ATG-treated rats. Serum creatinine levels were lower in rats that received ATG. Conclusion. ATG depleted the concentration of FKN, which inhibits migrations of DCs and macrophages into the kidney, and reduces IRI-related pathology.en_US
dc.identifier.doi10.1016/j.transproceed.2013.02.118
dc.identifier.endpage2468en_US
dc.identifier.issn0041-1345
dc.identifier.issn1873-2623
dc.identifier.issue6en_US
dc.identifier.pmid23953563en_US
dc.identifier.scopus2-s2.0-84882258053en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage2461en_US
dc.identifier.urihttps://dx.doi.org/10.1016/j.transproceed.2013.02.118
dc.identifier.urihttps://hdl.handle.net/20.500.12415/8519
dc.identifier.volume45en_US
dc.identifier.wosWOS:000323852000069en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherELSEVIER SCIENCE INCen_US
dc.relation.ispartofTRANSPLANTATION PROCEEDINGSen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmzKY03623
dc.titleA Novel Mechanism of Anti-T-Lymphocyte Globulin Mediated by Fractalkine in Renal Ischemia-Reperfusion Injury in Ratsen_US
dc.typeArticle
dspace.entity.typePublication

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