NF-kB and cytokines in pancreatic acinar cells.
10.3346/jkms.2000.15.S.S53
- Author:
Hyeyoung KIM
1
;
Jeong Yeon SEO
;
Kyung Hwan KIM
Author Information
1. Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea. kim626@yumc.yonsei.ac.kr
- Publication Type:Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
- Keywords:
NF-kB;
Cytokines;
Pancreatic Acinar Cells
- MeSH:
Acute Disease;
Chronic Disease;
Cytokines/immunology*;
Human;
NF-kappa B/metabolism*;
Pancreas/metabolism*;
Pancreas/immunology*;
Pancreas/cytology;
Pancreatitis/metabolism;
Pancreatitis/immunology;
Support, U.S. Gov't, Non-P.H.S.
- From:Journal of Korean Medical Science
2000;15(Suppl):S53-S54
- CountryRepublic of Korea
- Language:English
-
Abstract:
Reactive oxygen species (ROS), generated by infiltrating neutrophils, are considered as an important regulator in the pathogenesis and deveolpment of pancreatitis. A hallmark of the inflammatory response is the induction of cytokine gene expression, which may be regulated by oxidant-sensitive transcription factor, nuclear factor-kappaB (NF-KB). Present study aims to investigate whether neutrophils primed by 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA) affect the productions of H2O2 and lipid peroxide (LPO), NF-kappaB activation and cytokine production in pancreatic acinar cells, and whether these alterations were inhibited by N-acetylcysteine (NAC) and superoxide dismutase (SOD). ROS generation in neutrophils increased by PMA, which was inhibited by NAC and SOD. The productions of H2O2, LPO and TNF-alpha were increased with the amounts of PMA-primed neutrophils added to acinar cells while the productions of H2O2, LPO and cytokines increased with time. PMA-primed neutrophils resulted in the activation of two species of NF-kappaB dimers (a p50/p65 heterodimer and a p50 homodimer). Both NAC and SOD inhibited neutrophil-induced alterations in acinar cells. In conclusion, ROS, generated by neutrophils, activates NF-kappaB, resulting in upregulation of inflammatory cytokines in acinar cells. Antioxidants such as NAC might be clinically useful antiinflammatory agents by inhibiting oxidant-mediated activation of NF-KB and decreasing cytokine production.
