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

Jeong Yeon Seo, Hyeyoung Kim, Jeong Taeg Seo, Kyung Hwan Kim

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

Reactive oxygen species are considered important regulators in the pathogenesis and in the development of pancreatitis. The transcription factor nuclear factor κB (NF-κB) 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-κB 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-κB 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-κB activation and cytokine production in acinar cells caused by PMA-primed neutrophils. In conclusion, oxidative stress activates NF-κB, 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.

Original languageEnglish
Pages (from-to)63-70
Number of pages8
JournalPharmacology
Volume64
Issue number2
DOIs
Publication statusPublished - 2002 Feb 11

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Acinar Cells
Oxidative Stress
Antioxidants
Cytokines
Oxidants
Superoxide Dismutase
Acetates
Neutrophils
Lipid Peroxides
Reactive Oxygen Species
Allopurinol
Xanthine Oxidase
Acetylcysteine
Carotenoids
Pancreatitis
Adenosine Diphosphate
Interleukin-6
Anti-Inflammatory Agents
Transcription Factors
Up-Regulation

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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abstract = "Reactive oxygen species are considered important regulators in the pathogenesis and in the development of pancreatitis. The transcription factor nuclear factor κB (NF-κB) 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-κB 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-κB 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-κB activation and cytokine production in acinar cells caused by PMA-primed neutrophils. In conclusion, oxidative stress activates NF-κB, 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.",
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Oxidative stress induced cytokine production in isolated rat pancreatic acinar cells : Effects of small-molecule antioxidants. / Seo, Jeong Yeon; Kim, Hyeyoung; Seo, Jeong Taeg; Kim, Kyung Hwan.

In: Pharmacology, Vol. 64, No. 2, 11.02.2002, p. 63-70.

Research output: Contribution to journalArticle

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AB - Reactive oxygen species are considered important regulators in the pathogenesis and in the development of pancreatitis. The transcription factor nuclear factor κB (NF-κB) 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-κB 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-κB 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-κB activation and cytokine production in acinar cells caused by PMA-primed neutrophils. In conclusion, oxidative stress activates NF-κB, 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.

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