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TNF-α/cycloheximide-induced oxidative stress and apoptosis in murine intestinal epithelial MODE-K cells

Dinesh Babu UGent, Stefaan Soenen UGent, Koen Raemdonck UGent, Georges Leclercq UGent, OLE DE BACKER UGent, Roberto Motterlini and Romain Lefebvre UGent (2012) CURRENT PHARMACEUTICAL DESIGN. 18(28). p.4414-4425
abstract
In the mouse postoperative ileus model, we have shown an increase in oxidative stress after intestinal manipulation occurring earlier in the mucosa than in the muscular layer, which might contribute to epithelial barrier dysfunction. To address these findings in vitro, we assessed TNF-alpha/cycloheximide (CHX)-induced oxidative stress and apoptosis in a mouse intestinal epithelial cell line, MODE-K. The influence of heme oxygenase (HO)-1-related products and agents known to reduce reactive oxygen species (ROS) production on TNF-alpha/CHX-induced oxidative stress and apoptosis were investigated. MODE-K cells were exposed to different concentrations of TNF-alpha/CHX in the absence/presence of the test agents. Cell viability, caspase-3/7 activity, apoptosis, reduced glutathione level (GSH) and intracellular ROS production were measured. TNF-alpha/CHX decreased cell viability, increased caspase-3/7 activity, induced apoptosis, reduced the GSH level and increased ROS production in a concentration-dependent manner in MODE-K cells. All these effects of TNF-alpha/CHX were partially prevented by pretreatment with a carbon monoxide-releasing agent (CORM-A1) and nitrite. The antioxidant resveratrol abolished TNF-alpha/CHX-induced increase in ROS production and caspase-3/7 activity, but apoptosis was only partially prevented. MODE-K cells are sensitive to TNF-alpha-induced apoptosis in the presence of CHX, which is associated with increased intracellular ROS production and caspase-3/7 activation. The effects were partially mitigated by CORM-A1, nitrite and resveratrol. Thus, these agents could be of potential use in protecting the epithelial barrier against oxidative stress during intestinal ischemia/reperfusion injury.
Please use this url to cite or link to this publication:
author
organization
alternative title
TNF-alpha/cycloheximide-induced oxidative stress and apoptosis in murine intestinal epithelial MODE-K cells
year
type
journalArticle (original)
publication status
published
subject
keyword
TNF-alpha/CHX, MODE-K cells, ROS, apoptosis, bilirubin, CORM-A1, nitrite, resveratrol, NECROSIS-FACTOR-ALPHA, MONOXIDE-RELEASING MOLECULE, HEME OXYGENASE-1/CARBON MONOXIDE, CARBON-MONOXIDE, INFLAMMATORY RESPONSE, NITRIC-OXIDE, ISCHEMIA/REPERFUSION INJURY, GASTROINTESTINAL MOTILITY, POSTOPERATIVE ILEUS, CYTOCHROME-C
journal title
CURRENT PHARMACEUTICAL DESIGN
Curr. Pharm. Design
volume
18
issue
28
pages
4414 - 4425
Web of Science type
Review
Web of Science id
000307873900010
JCR category
PHARMACOLOGY & PHARMACY
JCR impact factor
3.311 (2012)
JCR rank
65/259 (2012)
JCR quartile
2 (2012)
ISSN
1381-6128
DOI
10.2174/138161212802481291
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2141216
handle
http://hdl.handle.net/1854/LU-2141216
date created
2012-06-13 08:38:12
date last changed
2013-10-01 00:30:34
@article{2141216,
  abstract     = {In the mouse postoperative ileus model, we have shown an increase in oxidative stress after intestinal manipulation occurring earlier in the mucosa than in the muscular layer, which might contribute to epithelial barrier dysfunction. To address these findings in vitro, we assessed TNF-alpha/cycloheximide (CHX)-induced oxidative stress and apoptosis in a mouse intestinal epithelial cell line, MODE-K. The influence of heme oxygenase (HO)-1-related products and agents known to reduce reactive oxygen species (ROS) production on TNF-alpha/CHX-induced oxidative stress and apoptosis were investigated. MODE-K cells were exposed to different concentrations of TNF-alpha/CHX in the absence/presence of the test agents. Cell viability, caspase-3/7 activity, apoptosis, reduced glutathione level (GSH) and intracellular ROS production were measured. TNF-alpha/CHX decreased cell viability, increased caspase-3/7 activity, induced apoptosis, reduced the GSH level and increased ROS production in a concentration-dependent manner in MODE-K cells. All these effects of TNF-alpha/CHX were partially prevented by pretreatment with a carbon monoxide-releasing agent (CORM-A1) and nitrite. The antioxidant resveratrol abolished TNF-alpha/CHX-induced increase in ROS production and caspase-3/7 activity, but apoptosis was only partially prevented. MODE-K cells are sensitive to TNF-alpha-induced apoptosis in the presence of CHX, which is associated with increased intracellular ROS production and caspase-3/7 activation. The effects were partially mitigated by CORM-A1, nitrite and resveratrol. Thus, these agents could be of potential use in protecting the epithelial barrier against oxidative stress during intestinal ischemia/reperfusion injury.},
  author       = {Babu, Dinesh and Soenen, Stefaan and Raemdonck, Koen and Leclercq, Georges and DE BACKER, OLE and Motterlini, Roberto and Lefebvre, Romain},
  issn         = {1381-6128},
  journal      = {CURRENT PHARMACEUTICAL DESIGN},
  keyword      = {TNF-alpha/CHX,MODE-K cells,ROS,apoptosis,bilirubin,CORM-A1,nitrite,resveratrol,NECROSIS-FACTOR-ALPHA,MONOXIDE-RELEASING MOLECULE,HEME OXYGENASE-1/CARBON MONOXIDE,CARBON-MONOXIDE,INFLAMMATORY RESPONSE,NITRIC-OXIDE,ISCHEMIA/REPERFUSION INJURY,GASTROINTESTINAL MOTILITY,POSTOPERATIVE ILEUS,CYTOCHROME-C},
  language     = {eng},
  number       = {28},
  pages        = {4414--4425},
  title        = {TNF-\ensuremath{\alpha}/cycloheximide-induced oxidative stress and apoptosis in murine intestinal epithelial MODE-K cells},
  url          = {http://dx.doi.org/10.2174/138161212802481291},
  volume       = {18},
  year         = {2012},
}

Chicago
Babu, Dinesh, Stefaan Soenen, Koen Raemdonck, Georges Leclercq, OLE DE BACKER, Roberto Motterlini, and Romain Lefebvre. 2012. “TNF-α/cycloheximide-induced Oxidative Stress and Apoptosis in Murine Intestinal Epithelial MODE-K Cells.” Current Pharmaceutical Design 18 (28): 4414–4425.
APA
Babu, D., Soenen, S., Raemdonck, K., Leclercq, G., DE BACKER, O., Motterlini, R., & Lefebvre, R. (2012). TNF-α/cycloheximide-induced oxidative stress and apoptosis in murine intestinal epithelial MODE-K cells. CURRENT PHARMACEUTICAL DESIGN, 18(28), 4414–4425.
Vancouver
1.
Babu D, Soenen S, Raemdonck K, Leclercq G, DE BACKER O, Motterlini R, et al. TNF-α/cycloheximide-induced oxidative stress and apoptosis in murine intestinal epithelial MODE-K cells. CURRENT PHARMACEUTICAL DESIGN. 2012;18(28):4414–25.
MLA
Babu, Dinesh, Stefaan Soenen, Koen Raemdonck, et al. “TNF-α/cycloheximide-induced Oxidative Stress and Apoptosis in Murine Intestinal Epithelial MODE-K Cells.” CURRENT PHARMACEUTICAL DESIGN 18.28 (2012): 4414–4425. Print.