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Oxidative stress-induced cytokine production in isolated rat pancreatic acinar cells: Effects of small-molecule antioxidants

Authors
 Jeong Yeon Seo  ;  Hyeyoung Kim  ;  Jeong Taeg Seo  ;  Kyung Hwan Kim 
Citation
 PHARMACOLOGY, Vol.64(2) : 63-70, 2002 
Journal Title
 PHARMACOLOGY 
ISSN
 0031-7012 
Issue Date
2002
MeSH
Adenosine Diphosphate/administration & dosage ; Animals ; Antioxidants/metabolism ; Antioxidants/pharmacology* ; Cytokines/biosynthesis* ; Hydrogen Peroxide/pharmacology ; Hypoxanthine/administration & dosage ; Iron Compounds/administration & dosage ; Lipid Peroxides/biosynthesis ; Male ; NF-kappa B/metabolism ; Neutrophils/drug effects ; Neutrophils/metabolism ; Oxidative Stress/drug effects* ; Pancreas/cytology ; Pancreas/drug effects* ; Pancreas/metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase/pharmacology ; Tetradecanoylphorbol Acetate/pharmacology ; Xanthine Oxidase/administration & dosage
Keywords
Oxidative stress ; Cytokines ; Pancreatic acinar cells
Abstract
Reactive oxygen species are considered important regulators in the pathogenesis and in the development of pancreatitis. The transcription factor nuclear factor ĸB (NF-ĸB) is activated by reactive oxygen species and regulates the gene expressions of inflammatory cytokines. The present study investigates (1) the susceptibility of isolated rat pancreatic acinar cells to oxidant attacks produced by adenosine diphosphate/ferrous iron, hypoxanthine/xanthine oxidase, and neutrophils primed with 4β-phorbol 12β-myristate 13α-acetate (PMA) and (2) the potential of small-molecule antioxidants (N-acetylcysteine, β-carotene, rebamipide, allopurinol) and superoxide dismutase (SOD) to prevent such injury and oxidant-mediated NF-ĸB activation and inflammatory cytokine production in the cells. As a result, oxidative stress resulted in a time-dependent increase in lipid peroxide production in pancreatic acinar cells which was inhibited by small-molecule antioxidants and SOD. PMA-primed neutrophils induced NF-ĸB activation and increased the production of cytokines (IL-6, TNF-α) in the cells. This was in parallel with lipid peroxide production. Small-molecule antioxidants and SOD inhibited NF-ĸB activation and cytokine production in acinar cells caused by PMA-primed neutrophils. In conclusion, oxidative stress activates NF-ĸB, resulting in upregulation of inflammatory cytokines in pancreatic acinar cells. Small-molecule antioxidants might be clinically useful anti-inflammatory agents by inhibiting oxidant-induced cytokine production.
Full Text
http://www.karger.com/Article/Abstract/56152
DOI
10.1159/000056152
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Kyung Hwan(김경환)
Seo, Jeong Taeg(서정택) ORCID logo https://orcid.org/0000-0003-2697-0251
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/143398
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