Beraprost sodium, a prostacyclin (PGI) analogue, ameliorates lipopolysaccharide-induced cellular injury in lung alveolar epithelial cells
dc.authorid | VICIL, SINAN/0000-0002-0444-4771 | |
dc.authorwosid | Vicil, Sinan/A-6412-2016 | |
dc.contributor.author | Vicil, Sinan | |
dc.contributor.author | Erdogan, Suat | |
dc.date.accessioned | 2024-06-12T11:07:55Z | |
dc.date.available | 2024-06-12T11:07:55Z | |
dc.date.issued | 2015 | |
dc.department | Trakya Üniversitesi | en_US |
dc.description.abstract | Background/aim: Human alveolar epithelial cells play a critical role in the pathogenesis of lung diseases. The objective of this study is to determine the contribution of beraprost sodium, a prostaglandin I-2 (PGI(2)) analogue, to inflammatory 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 mu M beraprost sodium 30 min before stimulation with 1 mu g/mL LPS for 24 h. The 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: The 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-alpha and IL-1 beta 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 significantly reversed the inflammation and suppressed oxidative stress. Conclusion: These findings 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.sponsorship | Mustafa Kemal University (Hatay, Turkey) Scientific Research Projects Committee [03M0116] | en_US |
dc.description.sponsorship | This study was supported by the Mustafa Kemal University (Hatay, Turkey) Scientific Research Projects Committee (Project No. 03M0116). | en_US |
dc.identifier.doi | 10.3906/sag-1401-108 | |
dc.identifier.endpage | 290 | en_US |
dc.identifier.issn | 1300-0144 | |
dc.identifier.issn | 1303-6165 | |
dc.identifier.issue | 2 | en_US |
dc.identifier.pmid | 26084116 | en_US |
dc.identifier.scopus | 2-s2.0-84926358686 | en_US |
dc.identifier.scopusquality | Q3 | en_US |
dc.identifier.startpage | 284 | en_US |
dc.identifier.trdizinid | 170930 | en_US |
dc.identifier.uri | https://doi.org/10.3906/sag-1401-108 | |
dc.identifier.uri | https://search.trdizin.gov.tr/yayin/detay/170930 | |
dc.identifier.uri | https://hdl.handle.net/20.500.14551/22235 | |
dc.identifier.volume | 45 | en_US |
dc.identifier.wos | WOS:000352482000005 | en_US |
dc.identifier.wosquality | Q4 | en_US |
dc.indekslendigikaynak | Web of Science | en_US |
dc.indekslendigikaynak | Scopus | en_US |
dc.indekslendigikaynak | TR-Dizin | en_US |
dc.indekslendigikaynak | PubMed | en_US |
dc.language.iso | en | en_US |
dc.publisher | Tubitak Scientific & Technological Research Council Turkey | en_US |
dc.relation.ispartof | Turkish Journal Of Medical Sciences | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/openAccess | en_US |
dc.subject | Lung | en_US |
dc.subject | Epithelial Cells | en_US |
dc.subject | Beraprost Sodium | en_US |
dc.subject | Lipopolysaccharide | en_US |
dc.subject | Inflammation | en_US |
dc.subject | Oxidative Stress | en_US |
dc.subject | Vascular Endothelial-Cells | en_US |
dc.subject | Cyclic-Amp | en_US |
dc.subject | Oxidative Stress | en_US |
dc.subject | Stable Analog | en_US |
dc.subject | Inflammation | en_US |
dc.subject | Macrophages | en_US |
dc.subject | Signal | en_US |
dc.subject | Expression | en_US |
dc.subject | Receptor | en_US |
dc.title | Beraprost sodium, a prostacyclin (PGI) analogue, ameliorates lipopolysaccharide-induced cellular injury in lung alveolar epithelial cells | en_US |
dc.type | Article | en_US |