Protective Effect of Infliximab, a Tumor Necrosis Factor-Alfa Inhibitor, on Bleomycin-Induced Lung Fibrosis in Rats

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dc.authorid0000-0003-2112-4056
dc.authorscopusid54892706700
dc.authorscopusid36023238400
dc.authorscopusid24436194200
dc.authorscopusid56715752200
dc.authorscopusid7102765266
dc.authorscopusid56810869000
dc.authorscopusid56768008500
dc.authorwosidAktas, Cevat/D-8468-2011
dc.authorwosidBilir, Bülent/AAK-5656-2021
dc.contributor.authorAltıntaş, Nejat
dc.contributor.authorErboğa, Mustafa
dc.contributor.authorAktaş, Cevat
dc.contributor.authorBilir, Bülent
dc.contributor.authorAydın, Murat
dc.contributor.authorŞengül, Aysun
dc.contributor.authorGürel, Ahmet
dc.contributor.authorTopçu, Birol
dc.date.accessioned2022-05-11T14:07:36Z
dc.date.available2022-05-11T14:07:36Z
dc.date.issued2016
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Göğüs Hastalıkları Ana Bilim Dalı
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalı
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, İç Hastalıkları Ana Bilim Dalı
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Tıbbi Biyokimya Ana Bilim Dalı
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Biyoistatistik Ana Bilim Dalı
dc.description.abstractWe aimed to investigate the preventive effect of Infliximab (IFX), a tumor necrosis factor (TNF)-alpha inhibitor, on bleomycin (BLC)-induced lung fibrosis in rats. Rats were assigned into four groups as follows: I-BLC group, a single intra-tracheal BLC (2.5 mg/kg) was installed; II-control group, a single intra-tracheal saline was installed; III-IFX + BLC group, a single-dose IFX (7 mg/kg) was administered intraperitoneally (i.p.), 72 h before the intra-tracheal BLC installation; IV-IFX group, IFX (7 mg/kg) was administered alone i.p. on the same day with IFX + BLC group. All animals were sacrificed on the 14th day of BLC installation. Levels of tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, interleukin (IL)-6, periostin, YKL-40, nitric oxide (NO) in rat serum were measured, as well as, myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity, and reduced glutathione (GSH), hydroxyproline, malondialdehyde (MDA) content in lung homogenates. Lung tissues were stained with hematoxylin and eosin (H&E) for quantitative histological evaluation. The inducible nitric oxide synthase (iNOS) expression and cell apoptosis in the lung tissues were determined quantitatively by immunohistochemical staining (INOS) and by TUNNEL staining, respectively. BLC installation worsened antioxidant status (such as SOD, CAT, GPx, GSH, MPO), while it increased the serum TNF-alpha, TGF-beta, IL-6, periostin, YKL-40, and lipid peroxidation, and collagen deposition, measured by MDA and hydroxyproline, respectively. IFX pretreatment improved antioxidant status as well as BLC-induced lung pathological changes, while it decreased the TNF-alpha, TGF-beta, IL-6, periostin, YKL-40, lipid peroxidation and collagen deposition. Finally, histological, immunohistochemical, and TUNNEL evidence also supported the ability of IFX to prevent BLC-induced lung fibrosis. The results of the present study indicate that IFX pretreatment can attenuate BLC-induced pulmonary fibrosis.
dc.description.sponsorshipNamik Kemal University, Scientific Research Projects UnitNamik Kemal University [NKUBAP.00.20.AR.1417]
dc.description.sponsorshipThe authors have no conflict of interest to declare. Funding for this study was received from Namik Kemal University, Scientific Research Projects Unit, Project No: NKUBAP.00.20.AR.1417
dc.identifier.doi10.1007/s10753-015-0224-z
dc.identifier.endpage78
dc.identifier.issn0360-3997
dc.identifier.issn1573-2576
dc.identifier.issue1en_US
dc.identifier.pmid26253295
dc.identifier.scopus2-s2.0-84958042151
dc.identifier.scopusqualityQ2
dc.identifier.startpage65
dc.identifier.urihttps://doi.org/10.1007/s10753-015-0224-z
dc.identifier.urihttps://hdl.handle.net/20.500.11776/5153
dc.identifier.volume39
dc.identifier.wosWOS:000370083500008
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorAltıntaş, Nejat
dc.institutionauthorErboğa, Mustafa
dc.institutionauthorAktaş, Cevat
dc.institutionauthorBilir, Bülent
dc.institutionauthorAydın, Murat
dc.institutionauthorGürel, Ahmet
dc.institutionauthorTopçu, Birol
dc.language.isoen
dc.publisherSpringer/Plenum Publishers
dc.relation.ispartofInflammation
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectidiopathic pulmonary fibrosis
dc.subjectinflammation
dc.subjectinfliximab
dc.subjectlung fibrosis
dc.subjecttransforming growth factor-beta
dc.subjecttumor necrosis factor-alpha
dc.subjecttumor necrosis factor-alpha inhibitors
dc.subjectInduced Pulmonary-Fibrosis
dc.subjectRheumatoid-Arthritis
dc.subjectGrowth-Factor
dc.subjectCollagen
dc.subjectTherapy
dc.subjectInjury
dc.subjectTnf
dc.subjectExpression
dc.subjectRecommendations
dc.subjectCytokines
dc.titleProtective Effect of Infliximab, a Tumor Necrosis Factor-Alfa Inhibitor, on Bleomycin-Induced Lung Fibrosis in Rats
dc.typeArticle

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