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dc.contributor.authorAtes, Gulten
dc.contributor.authorOzkok, Elif
dc.contributor.authorTamer, Sule
dc.contributor.authorKaptan, Engin
dc.contributor.authorYorulmaz, Hatice
dc.date.accessioned2021-03-05T14:01:01Z
dc.date.available2021-03-05T14:01:01Z
dc.identifier.citationYorulmaz H., Ozkok E., Kaptan E., Ates G., Tamer S., "Therapeutic effects of simvastatin on Galectin-3 and oxidative stress parameters in endotoxemic lung tissue", BIOSCIENCE REPORTS, cilt.38, 2018
dc.identifier.issn0144-8463
dc.identifier.othervv_1032021
dc.identifier.otherav_b5003264-2c3c-48fe-bcf1-fd42f60539c0
dc.identifier.urihttp://hdl.handle.net/20.500.12627/120542
dc.identifier.urihttps://doi.org/10.1042/bsr20180308
dc.description.abstractGalectins constitute of a soluble mammalian beta-galactoside binding lectin family, which play homeostatic roles in the regulation of the cell cycle, and apoptosis, in addition to their inflammatory conditions. Galectin-3 has an important role in the regulation of various inflammatory conditions including endotoxemia, and airway inflammation. Statins, the key precursor inhibitors of 3-hydroxyl-3-methyl coenzyme A (HMG-CoA) reductase, may prevent the progression of inflammation in sepsis after prior statin treatment. Endotoxemia leads to the formation of oxidative stress parameters in proteins, carbohydrates, and DNA. In the present study, we aimed to show the effects of simvastatin on Galectin-3, and glutathione reductase (GR), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS) levels in lung tissue of rats which were treated with lipopolysaccharides (LPS) during the early phase of sepsis. Rats were divided into four groups as the control, LPS (20 mg/kg), simvastatin (20 mg/kg), and simvastatin+LPS group. Galectin-3 expression in formalin-fixed paraffin-embedded lung tissue sections was demonstrated by using the immunohistochemistry methods. There were reduced densities, and the decreased number of Galectin-3 immunoreactivities in the simvastatin+ LPS group compared with the LPS group in the pneumocytes, and in the bronchial epithelium of lung tissue. In the LPS group, GR, GSH-Px, and SOD were found lower than the levels in simvastatin-treated LPS group (P<0.05, P<0.01, P<0.01 respectively) in the lung tissue. However, TBARS decreased in the simvastatin+ LPS group compared with the levels in LPS group (P<0.001). Simvastatin attenuates LPS-induced oxidative acute lung inflammation, oxidative stress, and suppresses LPS-induced Galectin-3 expression in the lung tissue.
dc.language.isoeng
dc.subjectHistoloji-Embriyoloji
dc.subjectYaşam Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectSitogenetik
dc.subjectTemel Bilimler
dc.subjectSağlık Bilimleri
dc.subjectTemel Tıp Bilimleri
dc.subjectTıp
dc.subjectHÜCRE BİYOLOJİSİ
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectBİYOKİMYA VE MOLEKÜLER BİYOLOJİ
dc.titleTherapeutic effects of simvastatin on Galectin-3 and oxidative stress parameters in endotoxemic lung tissue
dc.typeMakale
dc.relation.journalBIOSCIENCE REPORTS
dc.contributor.departmentHaliç Üniversitesi , ,
dc.identifier.volume38
dc.contributor.firstauthorID253593


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