The influence of irradiation on the potential chondroprotective effect of aqueous extract of propolis in rats.

摘要

PURPOSE: Cartilage degradation usually results as a consequence of inflammatory processes in the joints. To study this phenomenon experimentally, adjuvant-induced arthritis (AIA) was used as a model of chronic inflammation under the influence of irradiation. The potential chondroprotective effect of 13% aqueous extract of propolis (AEP) in arthritic rats was investigated. MATERIALS AND METHODS: The influence of whole body irradiation on the arthritic inflammatory response was investigated by subjecting rats to a Gamma source before the induction of arthritis. 13% AEP was injected intraperitoneally in a dose of 5 ml/kg and diclofenac was used as reference non-steroidal anti-inflammatory drug (NSAID) in a dose of 3 mg/kg. The chosen parameters for cartilage integrity were glycosaminoglycan (GAG), hydroxyproline contents in cartilage and cartilage oligomeric matrix protein (COMP) in serum. The serum levels of tumour necrosis factor-alpha (TNF-alpha), nitric oxide (NO) and the oxidative stress biomarkers such as blood glutathione (GSH) and plasma malondialdehyde (MDA) levels. RESULTS: Induction of arthritis led to a reduction in GAG and hydroxyproline content of femoral cartilage and a corresponding rise in COMP in serum. Previous exposure to irradiation resulted in a milder reduction of GAG and hydroxyproline and a lesser rise in COMP. Treatment of arthritic irradiated and non-irradiated rats with 13% AEP markedly prevented the breakdown of cartilage in a much more effective manner than diclofenac. Both AEP and diclofenac were equipotent in reducing the level of TNF-alpha and were able to normalize NO and the oxidative stress biomarkers in non-irradiated and irradiated arthritic rats. CONCLUSION: The ability of propolis to protect cartilage degradation could therefore prove of value in the treatment of chronic arthritic diseases, offering an advantage over some NSAID, particularly those with a potential detrimental effect on cartilage integrity.