Renoprotective Effects of Carbon Monoxide-Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity.
DC Field | Value | Language |
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dc.contributor.author | Yoon,YoonEun | - |
dc.contributor.author | Lee, Kwang Suk | - |
dc.contributor.author | Lee, Yong-Joon | - |
dc.contributor.author | Lee, Hyeon-Hui | - |
dc.contributor.author | Han, Woong Kyu | - |
dc.date.accessioned | 2022-07-14T01:52:01Z | - |
dc.date.available | 2022-07-14T01:52:01Z | - |
dc.date.created | 2021-05-14 | - |
dc.date.issued | 2017-06 | - |
dc.identifier.issn | 0041-1345 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/152140 | - |
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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.title | Renoprotective Effects of Carbon Monoxide-Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity. | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Yoon,YoonEun | - |
dc.identifier.doi | 10.1016/j.transproceed.2017.03.067 | - |
dc.identifier.scopusid | 2-s2.0-85020219403 | - |
dc.identifier.wosid | 000403382400054 | - |
dc.identifier.bibliographicCitation | TRANSPLANTATION PROCEEDINGS, v.49, no.5, pp.1175 - 1182 | - |
dc.relation.isPartOf | TRANSPLANTATION PROCEEDINGS | - |
dc.citation.title | TRANSPLANTATION PROCEEDINGS | - |
dc.citation.volume | 49 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 1175 | - |
dc.citation.endPage | 1182 | - |
dc.type.rims | ART | - |
dc.type.docType | 정기학술지(Article(Perspective Article포함)) | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalResearchArea | Surgery | - |
dc.relation.journalResearchArea | Transplantation | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.relation.journalWebOfScienceCategory | Surgery | - |
dc.relation.journalWebOfScienceCategory | Transplantation | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S0041134517302877?via%3Dihub | - |
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