Beraprost sodium, a prostacyclin (PGI) analogue, ameliorates lipopolysaccharide-induced cellular injury in lung alveolar epithelial cells

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dc.contributor.authorVıcıl, Sinan
dc.contributor.authorErdoğan, Suat
dc.date.accessioned2019-07-16T16:00:37Z
dc.date.available2019-07-16T16:00:37Z
dc.date.issued2015
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractBackground/aim: Human alveolar epithelial cells play a critical role in the pathogenesis of lung diseases. Te objective of this study is to determine the contribution of beraprost sodium, a prostaglandin I2 (PGI2) analogue, to infammatory and oxidative events in response to lipopolysaccharide (LPS) in airway epithelial cells. Materials and methods: Human pulmonary alveolar epithelial cells (A549) were pretreated with 10 µM beraprost sodium 30 min before stimulation with 1 µg/mL LPS for 24 h. Te cellular viability assessments were evaluated by quantitative MTT test. Catalase activity and glutathione and lipid peroxidation levels were determined using spectrophotometric techniques. mRNA expression analyses were performed by real-time qRT-PCR. Results: Te endotoxin induced a dose-dependent increase in proliferation of the cells, which was suppressed by the beraprost sodium treatment. LPS increased the expressions of TNF-α and IL-1β genes by 8- and 2.5-fold, respectively. It also induced lipid peroxidation and depleted cellular antioxidant capacity. Pretreatments of the cells with beraprost sodium signifcantly reversed the infammation and suppressed oxidative stress. Conclusion: Tese fndings suggest that beraprost sodium will provide a pivotal molecular basis for the design of new therapeutic strategies to cure endotoxin-induced lung injury, although additional comprehensive studies are still required.en_US
dc.description.abstractBackground/aim: Human alveolar epithelial cells play a critical role in the pathogenesis of lung diseases. Te objective of this study is to determine the contribution of beraprost sodium, a prostaglandin I2 (PGI2) analogue, to infammatory and oxidative events in response to lipopolysaccharide (LPS) in airway epithelial cells. Materials and methods: Human pulmonary alveolar epithelial cells (A549) were pretreated with 10 µM beraprost sodium 30 min before stimulation with 1 µg/mL LPS for 24 h. Te cellular viability assessments were evaluated by quantitative MTT test. Catalase activity and glutathione and lipid peroxidation levels were determined using spectrophotometric techniques. mRNA expression analyses were performed by real-time qRT-PCR. Results: Te endotoxin induced a dose-dependent increase in proliferation of the cells, which was suppressed by the beraprost sodium treatment. LPS increased the expressions of TNF-α and IL-1β genes by 8- and 2.5-fold, respectively. It also induced lipid peroxidation and depleted cellular antioxidant capacity. Pretreatments of the cells with beraprost sodium signifcantly reversed the infammation and suppressed oxidative stress. Conclusion: Tese fndings suggest that beraprost sodium will provide a pivotal molecular basis for the design of new therapeutic strategies to cure endotoxin-induced lung injury, although additional comprehensive studies are still required.en_US
dc.identifier.endpage290en_US
dc.identifier.issn1300-0144
dc.identifier.issue2en_US
dc.identifier.pmid26084116en_US
dc.identifier.scopus2-s2.0-84926358686en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage284en_US
dc.identifier.urihttps://trdizin.gov.tr/publication/paper/detail/TVRjd09UTXdNQT09
dc.identifier.urihttps://hdl.handle.net/20.500.12483/2425
dc.identifier.volume45en_US
dc.identifier.wosWOS:000352482000005en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakTR-Dizinen_US
dc.language.isoenen_US
dc.relation.ispartofTurkish Journal of Medical Sciencesen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US]
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCerrahien_US
dc.titleBeraprost sodium, a prostacyclin (PGI) analogue, ameliorates lipopolysaccharide-induced cellular injury in lung alveolar epithelial cellsen_US
dc.typeArticleen_US

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