Korean J Med.
1997 Jan;52(1):32-41.
Nitric Oxide(NO) in Inflammatory Arthritis
- Affiliations
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- 1Department of Internal Medicine, Rheumatism Center, College of Medicine, Hanyang University, Seoul, Korea.
- 2Institute of Rheumatology, College of Medicine, Hanyang University, Seoul, Korea.
Abstract
OBJECTIVES
Nitric Oxide(NO) is a toxic, inorganic, gaseous free radical produced during the metabolism of L-Arginine by NO synthase(NOS). It has been implicated in a rapidly growing number of physiological and pathophysiological processes such as cytotoxic effects against microbes and tumor cells, blood vessel dilation and neurotransmitter. Recently there is growing evidence implicating NO in immune regulation, inflammation, autoimmunity, and arthritis. We performed this study to determine a role for nitric oxide in inflammatory arthritis especially rheumatoid arthritis(RA).
METHODS
We measured (1) the concentrations of nitrite, a breakdown product of nitric oxide, in serum and synovial fluid from patients with RA and osteoarthritis(OA) and in the serum of controls (2) the concentrations of nitrite in the supernatant of cultured synovial tissue with RA and OA and (3) determined whether human chondrocytes and synoviocytes can synthesize nitric oxide and if so, how production is regulated by cytokines and antirheumatic drugs.
RESULTS
1) Serum nitrite concentrations in patients with RA and OA were higher than in controls. In both disease groups synovial fluid nitrite was higher than serum nitrite. Serum and synovial fluid nitrite concenrations in RA were higher than those in OA. However, those findings are not statistically significant. 2) Although these findings are not statistically significant, the concentration of nitrite in the supernatant of cultured synavial tissue with RA was higher than that in OA. 3) IL-1beta and TNF-alpah induced the biosynthesis of NO by chondrocytes and synoviocytes. IGF-1 and TGF-beta failed to provoke the production of NO. The biosynthesis of NO required an induction period of approximately 6 hours and was inhibited by L-NMMA and cycloheximide. Dexamethasone, indomethacin, gold sodium thiomalate and methotrexate had no effect on the induction of NO biosynthesis.
CONCLUSION
These results suggest a role for nitric oxide as an inflommatory mediator in inflammatory arthritis.
Keyword
MeSH Terms
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Antirheumatic Agents
Arginine
Arthritis*
Arthritis, Rheumatoid
Autoimmunity
Blood Cells
Chondrocytes
Cycloheximide
Cytokines
Dexamethasone
Gold Sodium Thiomalate
Humans
Indomethacin
Inflammation
Insulin-Like Growth Factor I
Metabolism
Methotrexate
Neurotransmitter Agents
Nitric Oxide
omega-N-Methylarginine
Synovial Fluid
Transforming Growth Factor beta
Antirheumatic Agents
Arginine
Cycloheximide
Cytokines
Dexamethasone
Gold Sodium Thiomalate
Indomethacin
Insulin-Like Growth Factor I
Methotrexate
Neurotransmitter Agents
Nitric Oxide
Transforming Growth Factor beta
omega-N-Methylarginine
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