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dc.contributor.authorSehitoglu, I.
dc.contributor.authorTumkaya, L.
dc.contributor.authorBedir, R.
dc.contributor.authorKalkan, Y.
dc.contributor.authorCure, M.C.
dc.contributor.authorYucel, A.F.
dc.contributor.authorCure, E.
dc.date.accessioned2020-12-19T20:17:17Z
dc.date.available2020-12-19T20:17:17Z
dc.date.issued2015
dc.identifier.issn0731-8898
dc.identifier.urihttps://doi.org/10.1615/JEnvironPatholToxicolOncol.2015012424
dc.identifier.urihttps://hdl.handle.net/11436/4365
dc.descriptionPubMed: 25746831en_US
dc.description.abstractIntroduction: Zoledronic acid (ZA), a bisphosphonate, increases the levels of cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-?), and reactive oxygen species (ROS) in subjects without cancer. Increased production of ROS, TNF-?, and IL-6 during ischemia and reperfusion (I/R) injury stimulates apoptosis that leads to renal injury. We aimed to investigate whether ZA treatment has a protective effect on renal tissues during I/R. Materials and Methods: Twenty-four Sprague-Dawley rats were used in this study, and they were subdivided randomly into three groups, each containing eight rats. Infrarenal abdominal aortic cross ligation was performed on the I/R group. After 2 h of ischemia, 2 h of reperfusion was applied. A single dose of 100 µg/kg ZA was administered intraperitoneally to the ZA group. I/R was performed after 48 h. Results: Whereas TNF-?, IL-6, and nitric oxide (NO) levels of the I/R group were higher than those of the control group, TNF-?, IL-6, and NO levels of the ZA group were higher than those of the I/R group [TNF-? (p=0.038), IL-6 (p=0.012), NO (p=0.002), and caspase-3 (p=0.037)] and the control group [TNF-? (p<0.001), IL-6 (p<0.001), NO (p<0.001), and caspase-3 (p<0.001)]. Whereas the carbonic anhydrase II (CA-II) level of the ZA group was lower than that of the control group (p=0.040), the CA-II level of the I/R group was higher than that of the control group (p=0.020). Conclusion: ZA may aggravate renal injury during I/R by increasing cytokine production and apoptosis. It may also increase renal injury and metabolic acidosis during I/R by suppressing CA-II enzyme activities. © 2015 by Begell House, Inc.en_US
dc.language.isoengen_US
dc.publisherBegell House Inc.en_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCarbonic anhydrase IIen_US
dc.subjectInterleukin-6en_US
dc.subjectIschemia/reperfusionen_US
dc.subjectKidneyen_US
dc.subjectZoledronic aciden_US
dc.titleZoledronic acid aggravates kidney damage during ischemia reperfusion injury in raten_US
dc.typearticleen_US
dc.contributor.departmentRTEÜen_US
dc.identifier.doi10.1615/JEnvironPatholToxicolOncol.2015012424
dc.identifier.volume34en_US
dc.identifier.issue1en_US
dc.identifier.startpage53en_US
dc.identifier.endpage61en_US
dc.relation.journalJournal of Environmental Pathology, Toxicology and Oncologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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