Department of Drug Radiation Research, National Centre for Radiation Research and Technology, Atomic Energy Authority, Egypt.
Int J Radiat Biol. 2011 Mar;87(3):254-62. doi: 10.3109/09553002.2011.530337. Epub 2010 Nov 19.
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.
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-α), nitric oxide (NO) and the oxidative stress biomarkers such as blood glutathione (GSH) and plasma malondialdehyde (MDA) levels.
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-α and were able to normalize NO and the oxidative stress biomarkers in non-irradiated and irradiated arthritic rats.
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.
软骨降解通常是关节炎症过程的结果。为了在实验中研究这种现象,采用佐剂诱导关节炎(AIA)作为在辐射影响下的慢性炎症模型。研究了 13%蜂胶水提取物(AEP)对关节炎大鼠的潜在软骨保护作用。
在关节炎诱导前,通过将大鼠置于伽马源下,研究全身照射对关节炎炎症反应的影响。以 5ml/kg 的剂量腹腔注射 13%AEP,以双氯芬酸作为参考非甾体抗炎药(NSAID),剂量为 3mg/kg。选择用于软骨完整性的参数为糖胺聚糖(GAG)、软骨中羟脯氨酸含量和血清中的软骨寡聚基质蛋白(COMP)。血清中肿瘤坏死因子-α(TNF-α)、一氧化氮(NO)和氧化应激生物标志物如血液谷胱甘肽(GSH)和血浆丙二醛(MDA)水平。
关节炎的诱导导致股骨软骨中 GAG 和羟脯氨酸含量减少,血清中 COMP 相应增加。先前暴露于辐射导致 GAG 和羟脯氨酸的减少减轻,COMP 的增加减少。用 13%AEP 治疗关节炎照射和未照射大鼠可显著防止软骨分解,效果比双氯芬酸更明显。AEP 和双氯芬酸在降低 TNF-α水平方面具有同等效力,能够使非照射和照射关节炎大鼠的 NO 和氧化应激生物标志物正常化。
因此,蜂胶保护软骨降解的能力可能在治疗慢性关节炎疾病方面具有价值,与某些 NSAID 相比具有优势,特别是对软骨完整性有潜在不利影响的 NSAID。