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dc.contributor.authorAlpertunga, B.
dc.contributor.authorJannuzzi, Ayşe Tarbın
dc.contributor.authorKara, Mehtap
dc.date.accessioned2021-03-03T13:05:44Z
dc.date.available2021-03-03T13:05:44Z
dc.date.issued2018
dc.identifier.citationJannuzzi A. T. , Kara M., Alpertunga B., "Celastrol ameliorates acetaminophen-induced oxidative stress and cytotoxicity in HepG2 cells", HUMAN & EXPERIMENTAL TOXICOLOGY, cilt.37, sa.7, ss.742-751, 2018
dc.identifier.issn0960-3271
dc.identifier.otherav_31f231a8-dd1b-4018-934f-6e962edeb2fa
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/37939
dc.identifier.urihttps://doi.org/10.1177/0960327117734622
dc.description.abstractAcetaminophen (APAP) is the most commonly used analgesic and antipyretic drug in the world. However, hepatotoxicity caused by APAP overdose is the most frequent cause of acute liver failure worldwide and oxidative stress involved in the pathogenesis of APAP hepatotoxicity. Celastrol is a natural triterpenoid derived from Tripterygium wilfordii Hook F. that exhibits antioxidant, anti-inflammatory, and antitumor activities. In this study, we aimed to investigate the potential ameliorative effects of celastrol against APAP-induced cytotoxicity and oxidative stress. Human hepatocellular carcinoma cells (HepG2) were incubated with 20 mM of APAP for 24 h and posttreated with 50 nM, 100 nM, or 200 nM of celastrol for a further 24 h. The methylthiazolyldiphenyl-tetrazolium bromide, lactate dehydrogenase, and neutral red uptake assays showed celastrol posttreatments recovered cell viability and cell membrane integrity in a concentration-dependent manner. Celastrol posttreatments exerted a significant increase in the glutathione content and a decrease in the malondialdehyde and protein carbonylation levels. Also, celastrol posttreatments attenuated the APAP-induced oxidative stress by raising glutathione peroxidase, glutathione reductase, and catalase activities. However, superoxide dismutase activity did not change. In conclusion, celastrol treatment may improve cell viability and increase cellular antioxidant defense in HepG2 cells. These results suggest that celastrol may have the potential to ameliorate the APAP-induced oxidative stress and cytotoxicity.
dc.language.isoeng
dc.subjectTemel Bilimler
dc.subjectEczacılık
dc.subjectYaşam Bilimleri
dc.subjectMeslek Bilimleri
dc.subjectFarmasötik Toksikoloji
dc.subjectSağlık Bilimleri
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectFarmakoloji ve Toksikoloji
dc.subjectTOKSİKOLOJİ
dc.titleCelastrol ameliorates acetaminophen-induced oxidative stress and cytotoxicity in HepG2 cells
dc.typeMakale
dc.relation.journalHUMAN & EXPERIMENTAL TOXICOLOGY
dc.contributor.departmentİstanbul Üniversitesi , ,
dc.identifier.volume37
dc.identifier.issue7
dc.identifier.startpage742
dc.identifier.endpage751
dc.contributor.firstauthorID83726


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