Caffeic acid phenethyl ester protects lung alveolar epithelial cells from cigarette smoke-induced damage

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dc.authoridBARLAS, Firat Baris/0000-0001-6401-686X
dc.authorwosidBARLAS, Firat Baris/ABB-1223-2020
dc.contributor.authorBarlas, Firat Baris
dc.contributor.authorErdogan, Suat
dc.date.accessioned2024-06-12T10:55:28Z
dc.date.available2024-06-12T10:55:28Z
dc.date.issued2015
dc.departmentTrakya Üniversitesien_US
dc.description.abstractBackground/aim: To evaluate the influence of caffeic acid phenethyl ester (CAPE) on cigarette smoke (CS)-induced cell damage, oxidative stress, and inflammation in human alveolar epithelial cells. Materials and methods: A549 alveolar epithelial cells were divided into control, CS exposure, CAPE, and CS+CAPE treatment groups. Undiluted CS-exposed medium (100%) and three dilutions (50%, 25%, and 10%) of CS-exposed media were applied to cultured A549 cells, which were analyzed after 3 h of incubation. Viability was measured by MTT assay, the gene expressions were evaluated by real-time PCR, and spectrophotometric techniques were used for biochemical assessments. Results: While CS exposure markedly reduced cellular viability by 32% after 3 h of incubation, 2.5 mu M CAPE treatments prevented CS-induced cell death by 40% in the cells. CS exposure triggered lipid peroxidation and depleted antioxidant capacity through inhibiting catalase activity and depleting glutathione levels. Moreover, CS increased nitric oxide production via upregulation of iNOS expression. CAPE treatment significantly restored antioxidant capacity and prevented lipid peroxidation. Cigarette smoke exposure induced inflammation by significantly upregulating TNF-alpha, IL-1 beta, and COX-2 mRNA expressions (3-, 2- and 25-fold, respectively). CAPE treatment of A549 cells significantly reversed the inflammation. Conclusion: CAPE may potentially represent a new therapeutic option in the prevention of CS-induced lung damages.en_US
dc.description.sponsorshipMustafa Kemal University Scientific Research Projects Committee [1004Y0115]en_US
dc.description.sponsorshipThis study was supported by the Mustafa Kemal University (the former address of the corresponding author) Scientific Research Projects Committee (Project No. 1004Y0115).en_US
dc.identifier.doi10.3906/sag-1404-14
dc.identifier.endpage541en_US
dc.identifier.issn1300-0144
dc.identifier.issn1303-6165
dc.identifier.issue3en_US
dc.identifier.pmid26281316en_US
dc.identifier.scopus2-s2.0-84929744755en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage534en_US
dc.identifier.urihttps://doi.org/10.3906/sag-1404-14
dc.identifier.urihttps://hdl.handle.net/20.500.14551/19437
dc.identifier.volume45en_US
dc.identifier.wosWOS:000356357800009en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTubitak Scientific & Technological Research Council Turkeyen_US
dc.relation.ispartofTurkish Journal Of Medical Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCaffeic Acid Phenethyl Esteren_US
dc.subjectCAPEen_US
dc.subjectInflammationen_US
dc.subjectOxidative Stressen_US
dc.subjectCigarette Smokeen_US
dc.subjectA549en_US
dc.subjectOxidative Stressen_US
dc.subjectInflammationen_US
dc.subjectAntioxidanten_US
dc.subjectGlutathioneen_US
dc.subjectHomeostasisen_US
dc.subjectExpressionen_US
dc.subjectApoptosisen_US
dc.subjectExposureen_US
dc.subjectExtracten_US
dc.subjectAirwaysen_US
dc.titleCaffeic acid phenethyl ester protects lung alveolar epithelial cells from cigarette smoke-induced damageen_US
dc.typeArticleen_US

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