Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 윤영은 | - |
dc.date.accessioned | 2019-11-26T04:22:01Z | - |
dc.date.available | 2019-11-26T04:22:01Z | - |
dc.date.issued | 2017-06 | - |
dc.identifier.citation | TRANSPLANTATION PROCEEDINGS, v. 49, no. 5, page. 1175-1182 | en_US |
dc.identifier.issn | 0041-1345 | - |
dc.identifier.issn | 1873-2623 | - |
dc.identifier.uri | https://www.sciencedirect.com/science/article/abs/pii/S0041134517302877?via%3Dihub | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/114523 | - |
dc.description.abstract | Background. We investigated the effects of a soluble carbon monoxide-releasing molecule (CORM) in cisplatin-induced cytotoxicity and ischemia-reperfusion injury (IRI) in vitro.Methods. The effects of CORM-3 (12.5-200 mu M) were assessed in normal kidney epithelial cells (HK-2, LLC-PK1) and renal cancer cells (Caki-1, Caki-2) subjected to cisplatin (50-200 mu M) or IRI. To induce IRI, cells were placed in an anaerobic chamber (37 degrees C, 95% nitrogen, 5% carbon dioxide) for 48 hours. Cells were transferred to complete medium and incubated at 37 degrees C, 5% carbon dioxide for 6 hours. Cell viability (CCK assays), tumor necrosis factor (TNF)-alpha messenger RNA (mRNA) levels (quantitative reverse-transcriptase polymerase chain reaction), and protein expression of cleaved-caspase 3 and oxidative stress markers (including Erk1/2, JNK, and P38; Western blot) were assessed.Results. Viability after IRI was approximately 40% of control. Protective effects of CORM-3 in the IRI model were dose-dependent. Cell viability was 40% recovered in 200-mu M CORM-3-pretreated cells compared with control. The protective effects of CORM-3 in cells exposed to cisplatin for 24 hours were weaker than in the IRI model. TNF-alpha, mRNA was induced by stimulated IRI or cisplatin exposure; CORM-3 pretreatment attenuated the rise in TNF-alpha mRNA. IRI or cisplatin-induced activated oxidative stress markers decreased in CORM-3-pretreated cells. CORM-3 reduced expression of the apoptotic marker cleaved-caspase 3.Conclusion. Our data demonstrate the protective effects of CORM-3 in cisplatin cytotoxicity and IRI in both normal kidney cells and renal cancer cells in vitro. CORM-3 exerts these effects by ameliorating inflammatory and oxidative stress pathways. | en_US |
dc.description.sponsorship | This study was financially supported by the "Dongwha" Faculty Research Assistance Program of Yonsei University College of Medicine (6-2015-0170) and the National Research Foundation grant (NRF-2012R1A1A1042968) funded by the Korean government (MEST). The funding sources had no involvement in this study. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | ELSEVIER SCIENCE INC | en_US |
dc.subject | INDUCED APOPTOSIS | en_US |
dc.subject | CELL-DEATH | en_US |
dc.title | Renoprotective Effects of Carbon Monoxide-Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity. | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.1016/j.transproceed.2017.03.067 | - |
dc.relation.journal | TRANSPLANTATION PROCEEDINGS | - |
dc.contributor.googleauthor | Yoon, Y. E. | - |
dc.contributor.googleauthor | Lee, K. S. | - |
dc.contributor.googleauthor | Lee, Y. J. | - |
dc.contributor.googleauthor | Lee, H. H. | - |
dc.contributor.googleauthor | Han, W. K. | - |
dc.relation.code | 2017001147 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | urologistyoon | - |
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