Caffeic acid phenethyl ester ameliorates pulmonary inflammation and apoptosis reducing Nf-?? activation in blunt pulmonary contusion model

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dc.authorscopusid55838809000
dc.authorwosidkaraboga, ihsan/AAZ-9840-2020
dc.contributor.authorKaraboğa, İhsan
dc.date.accessioned2022-05-11T14:48:36Z
dc.date.available2022-05-11T14:48:36Z
dc.date.issued2019
dc.departmentYüksekokullar, Sağlık Yüksekokulu, Acil Yardım ve Afet Yönetimi Bölümü
dc.description.abstractBACKGROUND: Pulmonary contusion (PC) is an important life-threatening clinical condition characterized by lung injury and inflammation. Caffeic acid phenethyl ester (CAPE) is a biological agent with potent antioxidant and anti-inflammatory effects. This study aimed to investigate the potential effects of CAPE on tissue damage, nuclear factor kappa-beta (Nf-kappa beta) activity, inducible nitric oxide synthase (iNOS) synthesis, and pulmonary apoptosis in an experimental PC model. METHODS: Forty adult Wistar albino rats were used in this study and divided into four groups as follows: control, PC, PC + CAPE, and CAPE. CAPE was administered intraperitoneally for seven days following PC formation (10 jimol/kg, dissolved in dimethyl sulfoxide). Wet/dry weight ratio in lung tissue was determined. The pulmonary tissue was examined using hematoxylin-eosin and Masson's trichrome histochemical staining and also by scanning electron microscopy. Nf-kappa beta and iNOS activities in the lungs were determined by the indirect immunohistochemical method. Pulmonary apoptosis was detected by the TUNEL method. RESULTS: Increased leukocyte infiltration score, pulmonary edema, alveolar damage, and increased Nf-kappa beta and iNOS activities were determined in the PC group. CAPE administration inhibited Nf-kappa beta and iNOS activities and pulmonary apoptosis. CONCLUSION: In this study, the findings showed that CAPE inhibited tissue damage by suppressing inflammatory mediators of Nf-kappa beta and iNOS activities. Also, CAPE was found to be protective in the lung tissue and could be used as a therapeutic agent.
dc.description.sponsorshipTekirdag Namik Kemal University, Scientific Research Projects Commission [NKUBAP.23.GA.18.160]
dc.description.sponsorshipThis study was supported by Tekirdag Namik Kemal University, Scientific Research Projects Commission (NKUBAP.23.GA.18.160).
dc.identifier.doi10.5505/tjtes.2018.51694
dc.identifier.endpage439
dc.identifier.issn1306-696X
dc.identifier.issue5en_US
dc.identifier.pmid31475327
dc.identifier.scopus2-s2.0-85071737972
dc.identifier.scopusqualityQ2
dc.identifier.startpage433
dc.identifier.urihttps://doi.org/10.5505/tjtes.2018.51694
dc.identifier.urihttps://hdl.handle.net/20.500.11776/10662
dc.identifier.volume25
dc.identifier.wosWOS:000483463200002
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorKaraboğa, İhsan
dc.language.isoen
dc.publisherTurkish Assoc Trauma Emergency Surgery
dc.relation.ispartofUlusal Travma Ve Acil Cerrahi Dergisi-Turkish Journal of Trauma & Emergency Surgery
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectinflammation
dc.subjectiNOS
dc.subjectNf-kappa beta
dc.subjectpulmonary contusion
dc.subjectAcute Lung Injury
dc.subjectChest Trauma
dc.subjectOxidative Stress
dc.subjectNitric-Oxide
dc.subjectDexamethasone
dc.subjectRats
dc.subjectInhibition
dc.subjectCape
dc.titleCaffeic acid phenethyl ester ameliorates pulmonary inflammation and apoptosis reducing Nf-?? activation in blunt pulmonary contusion model
dc.title.alternativeCaffeic acid phenethyl ester ameliorates pulmonary inflammation and apoptosis reducing Nf-kappa beta activation in blunt pulmonary contusion model
dc.typeArticle

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