dc.contributor.author | Bolkent, Sehnaz | |
dc.contributor.author | Bayrak, Bertan Boran | |
dc.contributor.author | Oztay, Füsün | |
dc.contributor.author | Gezginci-Oktayoglu, Selda | |
dc.contributor.author | Yanardag, Refiye | |
dc.date.accessioned | 2021-03-06T07:52:17Z | |
dc.date.available | 2021-03-06T07:52:17Z | |
dc.identifier.citation | Oztay F., Gezginci-Oktayoglu S., Bayrak B. B. , Yanardag R., Bolkent S., "Cathepsin B inhibition improves lung injury associated to D-galactosamine/tumor necrosis factor-alpha-induced liver injury in mice.", Molecular and cellular biochemistry, cilt.333, ss.65-72, 2010 | |
dc.identifier.issn | 0300-8177 | |
dc.identifier.other | vv_1032021 | |
dc.identifier.other | av_de410dd9-0752-4fe9-8492-cbc220cc8c80 | |
dc.identifier.uri | http://hdl.handle.net/20.500.12627/146428 | |
dc.identifier.uri | https://doi.org/10.1007/s11010-009-0205-3 | |
dc.description.abstract | The present study was designed to investigate the effects of benzyloxicarbonyl-l-phenylalanyl-alanine-fluoromethylketone (Z-FA.FMK), an inhibitor of cathepsin B on lung injury that occurs concurrently with liver injury induced by d-galactosamine/tumor necrosis factor-alpha (d-GalN/TNF-alpha). Four groups of BALB/c male mice were treated as follows: Group 1-mice receiving intravenous (iv) injections of physiological saline; Group 2-administered with 8 mg/kg Z-FA.FMK by iv injection; Group 3-mice treated with 700 mg/kg d-GalN and 15 mu g/kg TNF-alpha by sequential intraperitoneal (ip) injection; Group 4-treated with 700 mg/kg d-GalN and 15 mu g/kg TNF-alpha by sequential ip injection 1 h after administration with 8 mg/kg Z-FA.FMK. Mice from Groups 3 and 4 were sacrificed 4 h after d-GalN/TNF-alpha injections. The mice treated with d-GalN/TNF-alpha showed lung damage; increased TNF receptor-associated factor immunoreactivity, lipid peroxidation, protein carbonyl content, and lactate dehydrogenase activity; decreased catalase, superoxide dismutase, and paraoxonase activities. Treatment with Z-FA.FMK resulted in an improvement of these alterations in d-GalN/TNF-alpha-administered mice. The apoptotic index of type-II pneumocytes was the almost same in the four study groups, but pneumocytes labeled with proliferating cell nuclear antigen antibody was more numerous in Group 4 mice. Our results show that d-GalN/TNF-alpha results in lung damage without induction of apoptosis. Treatment with Z-FA.FMK stimulates proliferation of type-II pneumocytes and improves degenerative alterations in injured lung occurred with liver injury induced by d-GalN/TNF-alpha. | |
dc.language.iso | eng | |
dc.subject | Yaşam Bilimleri | |
dc.subject | Moleküler Biyoloji ve Genetik | |
dc.subject | Temel Bilimler | |
dc.subject | Temel Tıp Bilimleri | |
dc.subject | Histoloji-Embriyoloji | |
dc.subject | Sağlık Bilimleri | |
dc.subject | Tıp | |
dc.subject | Yaşam Bilimleri (LIFE) | |
dc.subject | Moleküler Biyoloji ve Genetik | |
dc.subject | HÜCRE BİYOLOJİSİ | |
dc.title | Cathepsin B inhibition improves lung injury associated to D-galactosamine/tumor necrosis factor-alpha-induced liver injury in mice. | |
dc.type | Makale | |
dc.relation.journal | Molecular and cellular biochemistry | |
dc.contributor.department | İstanbul Üniversitesi , Mühendislik Fakültesi Kimya Bölümü , Kimya | |
dc.identifier.volume | 333 | |
dc.identifier.startpage | 65 | |
dc.identifier.endpage | 72 | |
dc.contributor.firstauthorID | 2179200 | |