Renoprotective Effects of Carbon Monoxide-Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity.
- Authors
- Yoon,YoonEun; Lee, Kwang Suk; Lee, Yong-Joon; Lee, Hyeon-Hui; Han, Woong Kyu
- Issue Date
- Jun-2017
- Publisher
- ELSEVIER SCIENCE INC
- Citation
- TRANSPLANTATION PROCEEDINGS, v.49, no.5, pp.1175 - 1182
- Indexed
- SCIE
SCOPUS
- Journal Title
- TRANSPLANTATION PROCEEDINGS
- Volume
- 49
- Number
- 5
- Start Page
- 1175
- End Page
- 1182
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/152140
- DOI
- 10.1016/j.transproceed.2017.03.067
- ISSN
- 0041-1345
- 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.
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