Effect of selective COX-2 inhibitor, celecoxib on adjuvant-induced arthritis model in irradiated rats

Purpose: The potential value of celecoxib was compared to a standard non-steroidal anti-inflammatory drug (NSAID), diclofenac in the adjuvant-induced arthritis (AIA) model in rats as a model of chronic inflammation under the influence of ionising radiation. Material and methods: Various inflammatory...

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Published in:International journal of radiation biology 2010-12, Vol.86 (12), p.1079-1087
Main Authors: EL-Ghazaly, Mona A., Nada, Ahmed S., EL-Hazek, Rania M., Khayyal, Mohamed T.
Format: Article
Language:English
Subjects:
adjuvant arthritis
Animals
Anti-Inflammatory Agents, Non-Steroidal - therapeutic use
Arthritis, Experimental - drug therapy
Arthritis, Experimental - etiology
Arthritis, Experimental - metabolism
Celecoxib
Cyclooxygenase 2 Inhibitors - therapeutic use
cyclooxygenase enzyme
cytokines
Diclofenac - therapeutic use
Inflammation Mediators - blood
Interleukin-1beta - blood
Interleukin-6 - blood
ionising radiation
Male
Oxidative Stress - drug effects
Oxidative Stress - radiation effects
Pyrazoles - therapeutic use
Rats
Rats, Wistar
reactive oxygen species
Space life sciences
Sulfonamides - therapeutic use
Tumor Necrosis Factor-alpha - blood
Whole-Body Irradiation
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Summary:Purpose: The potential value of celecoxib was compared to a standard non-steroidal anti-inflammatory drug (NSAID), diclofenac in the adjuvant-induced arthritis (AIA) model in rats as a model of chronic inflammation under the influence of ionising radiation. Material and methods: Various inflammatory mediators and biochemical parameters were measured in the arthritic rats under the influence of ionising radiation. Results: Exposure of the animals to a radiation dose of 2 Gy before inoculation of the adjuvant led to a marked increase in the paw volume reaching ca. 70% more than that in non-irradiated ones as well as a significant increase in the levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α), prostaglandin E2 (PGE2) as an index of cyclooxygenase-2 (COX-2) activity, thromboxane B2 (TXB2) as an index of cyclooxygenase-1 (COX-1) activity and plasma level of malondialdehyde (MDA). The blood glutathione (GSH) level was not affected by the dose of irradiation used while superoxidedismutase (SOD) activity was reduced. Treatment with celecoxib in a dose of 5 mg/kg was effective in decreasing the elevated levels of IL-6, IL-1β, TNF-α, PGE2 whereas it lacked any effect on TXB2 level since it had hardly any effect on COX-1 enzyme. Both drugs at the selected dose levels showed no effect on level of MDA, GSH and SOD activity. Conclusion: Irradiation of animals caused a marked change in the inflammatory response in AIA model of inflammation. Both celecoxib and diclofenac were nearly equipotent in suppressing the inflammatory response in both normal and irradiated rats. Accordingly, since the inhibition of COX-1 by traditional NSAID is thought to have undesirable side-effects on proliferating tissues, it would seem preferable to use selective COX-2 inhibitors to limit such deleterious effect.
ISSN:0955-3002
1362-3095
DOI:10.3109/09553002.2010.501839