Renoprotective Effects of Carbon Monoxide–Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity

Y. E. Yoon, K. S. Lee, Y. J. Lee, H. H. Lee, W. K. Han

Research output: Contribution to journalArticle

7 Citations (Scopus)

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 μM) were assessed in normal kidney epithelial cells (HK-2, LLC-PK1) and renal cancer cells (Caki-1, Caki-2) subjected to cisplatin (50–200 μM) or IRI. To induce IRI, cells were placed in an anaerobic chamber (37°C, 95% nitrogen, 5% carbon dioxide) for 48 hours. Cells were transferred to complete medium and incubated at 37°C, 5% carbon dioxide for 6 hours. Cell viability (CCK assays), tumor necrosis factor (TNF)-α 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-μM 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-α mRNA was induced by stimulated IRI or cisplatin exposure; CORM-3 pretreatment attenuated the rise in TNF-α 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.

Original languageEnglish
Pages (from-to)1175-1182
Number of pages8
JournalTransplantation Proceedings
Volume49
Issue number5
DOIs
Publication statusPublished - 2017 Jun

Fingerprint

Reperfusion Injury
Cisplatin
Carbon
Oxidative Stress
Tumor Necrosis Factor-alpha
Carbon Dioxide
Caspase 3
Messenger RNA
Cell Survival
Kidney
Kidney Neoplasms
Reverse Transcriptase Polymerase Chain Reaction
Renal Cell Carcinoma
Nitrogen
Western Blotting
Epithelial Cells

All Science Journal Classification (ASJC) codes

  • Surgery
  • Transplantation

Cite this

@article{5fb4d9ee44d24e4f91d194dd68643c73,
title = "Renoprotective Effects of Carbon Monoxide–Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity",
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 μM) were assessed in normal kidney epithelial cells (HK-2, LLC-PK1) and renal cancer cells (Caki-1, Caki-2) subjected to cisplatin (50–200 μM) or IRI. To induce IRI, cells were placed in an anaerobic chamber (37°C, 95{\%} nitrogen, 5{\%} carbon dioxide) for 48 hours. Cells were transferred to complete medium and incubated at 37°C, 5{\%} carbon dioxide for 6 hours. Cell viability (CCK assays), tumor necrosis factor (TNF)-α 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-μM 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-α mRNA was induced by stimulated IRI or cisplatin exposure; CORM-3 pretreatment attenuated the rise in TNF-α 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.",
author = "Yoon, {Y. E.} and Lee, {K. S.} and Lee, {Y. J.} and Lee, {H. H.} and Han, {W. K.}",
year = "2017",
month = "6",
doi = "10.1016/j.transproceed.2017.03.067",
language = "English",
volume = "49",
pages = "1175--1182",
journal = "Transplantation Proceedings",
issn = "0041-1345",
publisher = "Elsevier USA",
number = "5",

}

Renoprotective Effects of Carbon Monoxide–Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity. / Yoon, Y. E.; Lee, K. S.; Lee, Y. J.; Lee, H. H.; Han, W. K.

In: Transplantation Proceedings, Vol. 49, No. 5, 06.2017, p. 1175-1182.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Renoprotective Effects of Carbon Monoxide–Releasing Molecule 3 in Ischemia-Reperfusion Injury and Cisplatin-Induced Toxicity

AU - Yoon, Y. E.

AU - Lee, K. S.

AU - Lee, Y. J.

AU - Lee, H. H.

AU - Han, W. K.

PY - 2017/6

Y1 - 2017/6

N2 - 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 μM) were assessed in normal kidney epithelial cells (HK-2, LLC-PK1) and renal cancer cells (Caki-1, Caki-2) subjected to cisplatin (50–200 μM) or IRI. To induce IRI, cells were placed in an anaerobic chamber (37°C, 95% nitrogen, 5% carbon dioxide) for 48 hours. Cells were transferred to complete medium and incubated at 37°C, 5% carbon dioxide for 6 hours. Cell viability (CCK assays), tumor necrosis factor (TNF)-α 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-μM 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-α mRNA was induced by stimulated IRI or cisplatin exposure; CORM-3 pretreatment attenuated the rise in TNF-α 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.

AB - 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 μM) were assessed in normal kidney epithelial cells (HK-2, LLC-PK1) and renal cancer cells (Caki-1, Caki-2) subjected to cisplatin (50–200 μM) or IRI. To induce IRI, cells were placed in an anaerobic chamber (37°C, 95% nitrogen, 5% carbon dioxide) for 48 hours. Cells were transferred to complete medium and incubated at 37°C, 5% carbon dioxide for 6 hours. Cell viability (CCK assays), tumor necrosis factor (TNF)-α 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-μM 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-α mRNA was induced by stimulated IRI or cisplatin exposure; CORM-3 pretreatment attenuated the rise in TNF-α 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.

UR - http://www.scopus.com/inward/record.url?scp=85020219403&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85020219403&partnerID=8YFLogxK

U2 - 10.1016/j.transproceed.2017.03.067

DO - 10.1016/j.transproceed.2017.03.067

M3 - Article

C2 - 28583551

AN - SCOPUS:85020219403

VL - 49

SP - 1175

EP - 1182

JO - Transplantation Proceedings

JF - Transplantation Proceedings

SN - 0041-1345

IS - 5

ER -