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Differential effects of CORM-2 and CORM-401 in murine intestinal epithelial MODE-K cells under oxidative stress

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Abstract
Carbon monoxide (CO)-releasing molecules (CO-RMs) are intensively studied to provide cytoprotective and anti-inflammatory effects of CO in inflammatory conditions including intestinal inflammation. The water-soluble CORM-A1 reduced apoptosis and NADPH oxidase (NOX)-derived reactive oxygen species (ROS) induced by tumor necrosis factor (TNF)-alpha/cycloheximide (CHX) in mouse MODE-K intestinal epithelial cells (IECs), without influencing TNF-alpha/CHX-induced mitochondrial superoxide anion (O-2(center dot-)). The aim of the present study in the same model was to comparatively investigate the influence of lipid-soluble CORM-2 and water-soluble CORM-401, shown in vitro to release more CO under oxidative conditions. CORM-2 abolished TNF-alpha/CHX-induced total cellular ROS whereas CORM-401 partially reduced it, both partially reducing TNF-alpha/CHXinduced cell death. Only CORM-2 increased mitochondrial O-2(center dot-) production after 2 h of incubation. CORM-2 reduced TNF-alpha/CHX-, rotenone-and antimycin-A-induced mitochondrial O-2(center dot-) production; CORM-401 only reduced the effect of antimycin-A. Co-treatment with CORM-401 during 1 h exposure to H2O2 reduced H2O2 (7.5 mM)induced ROS production and cell death, whereas CORM-2 did not. The study illustrates the importance of the chemical characteristics of different CO-RMs. The lipid solubility of CORM-2 might contribute to its interference with TNF-alpha/CHX-induced mitochondrial ROS signaling, at least in mouse IECs. CORM-401 is more effective than other CO-RMs under H2O2-induced oxidative stress conditions.
Keywords
carbon monoxide-releasing molecules, hydrogen peroxide, intestinal epithelial cells, mitochondria, oxidative stress, reactive oxygen species, solubility, TNF-alpha/CHX, MONOXIDE-RELEASING MOLECULES, HYDROGEN-PEROXIDE PRODUCTION, CARBON-MONOXIDE, SUPEROXIDE ANION, IN-VIVO, THERAPEUTIC APPLICATIONS, ULCERATIVE-COLITIS, SPECIES FORMATION, HEME OXYGENASE, CO-RMS

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Citation

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Chicago
Babu, Dinesh, Georges Leclercq, Roberto Motterlini, and Romain Lefebvre. 2017. “Differential Effects of CORM-2 and CORM-401 in Murine Intestinal Epithelial MODE-K Cells Under Oxidative Stress.” Frontiers in Pharmacology 8.
APA
Babu, D., Leclercq, G., Motterlini, R., & Lefebvre, R. (2017). Differential effects of CORM-2 and CORM-401 in murine intestinal epithelial MODE-K cells under oxidative stress. FRONTIERS IN PHARMACOLOGY, 8.
Vancouver
1.
Babu D, Leclercq G, Motterlini R, Lefebvre R. Differential effects of CORM-2 and CORM-401 in murine intestinal epithelial MODE-K cells under oxidative stress. FRONTIERS IN PHARMACOLOGY. 2017;8.
MLA
Babu, Dinesh, Georges Leclercq, Roberto Motterlini, et al. “Differential Effects of CORM-2 and CORM-401 in Murine Intestinal Epithelial MODE-K Cells Under Oxidative Stress.” FRONTIERS IN PHARMACOLOGY 8 (2017): n. pag. Print.
@article{8508514,
  abstract     = {Carbon monoxide (CO)-releasing molecules (CO-RMs) are intensively studied to provide cytoprotective and anti-inflammatory effects of CO in inflammatory conditions including intestinal inflammation. The water-soluble CORM-A1 reduced apoptosis and NADPH oxidase (NOX)-derived reactive oxygen species (ROS) induced by tumor necrosis factor (TNF)-alpha/cycloheximide (CHX) in mouse MODE-K intestinal epithelial cells (IECs), without influencing TNF-alpha/CHX-induced mitochondrial superoxide anion (O-2(center dot-)). The aim of the present study in the same model was to comparatively investigate the influence of lipid-soluble CORM-2 and water-soluble CORM-401, shown in vitro to release more CO under oxidative conditions. CORM-2 abolished TNF-alpha/CHX-induced total cellular ROS whereas CORM-401 partially reduced it, both partially reducing TNF-alpha/CHXinduced cell death. Only CORM-2 increased mitochondrial O-2(center dot-) production after 2 h of incubation. CORM-2 reduced TNF-alpha/CHX-, rotenone-and antimycin-A-induced mitochondrial O-2(center dot-) production; CORM-401 only reduced the effect of antimycin-A. Co-treatment with CORM-401 during 1 h exposure to H2O2 reduced H2O2 (7.5 mM)induced ROS production and cell death, whereas CORM-2 did not. The study illustrates the importance of the chemical characteristics of different CO-RMs. The lipid solubility of CORM-2 might contribute to its interference with TNF-alpha/CHX-induced mitochondrial ROS signaling, at least in mouse IECs. CORM-401 is more effective than other CO-RMs under H2O2-induced oxidative stress conditions.},
  articleno    = {31},
  author       = {Babu, Dinesh and Leclercq, Georges and Motterlini, Roberto and Lefebvre, Romain},
  issn         = {1663-9812},
  journal      = {FRONTIERS IN PHARMACOLOGY},
  keyword      = {carbon monoxide-releasing molecules,hydrogen peroxide,intestinal epithelial cells,mitochondria,oxidative stress,reactive oxygen species,solubility,TNF-alpha/CHX,MONOXIDE-RELEASING MOLECULES,HYDROGEN-PEROXIDE PRODUCTION,CARBON-MONOXIDE,SUPEROXIDE ANION,IN-VIVO,THERAPEUTIC APPLICATIONS,ULCERATIVE-COLITIS,SPECIES FORMATION,HEME OXYGENASE,CO-RMS},
  language     = {eng},
  pages        = {17},
  title        = {Differential effects of CORM-2 and CORM-401 in murine intestinal epithelial MODE-K cells under oxidative stress},
  url          = {http://dx.doi.org/10.3389/fphar.2017.00031},
  volume       = {8},
  year         = {2017},
}

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