Goranov Nikolay V
Department of Veterinary Surgery, Faculty of Veterinary Medicine, Trakia University, Stara Zagora, Bulgaria.
Vet Clin Pathol. 2007 Jun;36(2):192-5. doi: 10.1111/j.1939-165x.2007.tb00208.x.
Chondrocyte lipid peroxidation is strongly suggested to mediate collagen degradation and thus, to be involved in the pathogenesis of cartilage degradation and osteoarthritis (OA).
The objective of this study was to evaluate early changes in serum biochemical indicators of oxidative stress during the development of OA in a canine model.
Experimental OA was induced in 7 dogs by transection of the anterior cruciate ligament (Pond-Nuki model). Venous blood samples were obtained prior to the operation and on postoperative days 30, 60, and 105. The activity of serum catalase (an antioxidant enzyme), malondialdehyde (MDA) concentration (a marker of lipid peroxidation), and serum C2C neoepitope concentration (a marker of collagen type II degradation) were measured.
A statistically significant increase in all parameters as early as the 30th postoperative day was observed, compared with preoperative values. Serum catalase activity peaked on day 60, whereas MDA and C2C concentrations increased continuously until the end of the experimental period. A significant positive correlation was found between MDA and C2C concentrations, but not between catalase activity and MDA or C2C concentrations.
The results support the hypothesis that oxidative stress is involved in the pathogenesis of OA in the dog based on the Pond-Nuki model. The correlation between MDA and C2C concentrations suggests a possible association between oxidative stress and cartilage degeneration.
强烈提示软骨细胞脂质过氧化介导胶原蛋白降解,因此参与软骨降解和骨关节炎(OA)的发病机制。
本研究的目的是评估犬类OA模型发展过程中氧化应激血清生化指标的早期变化。
通过切断前交叉韧带(Pond-Nuki模型)在7只犬中诱导实验性OA。在手术前以及术后第30、60和105天采集静脉血样本。测量血清过氧化氢酶(一种抗氧化酶)活性、丙二醛(MDA)浓度(脂质过氧化标志物)和血清C2C新表位浓度(II型胶原降解标志物)。
与术前值相比,早在术后第30天所有参数均有统计学显著增加。血清过氧化氢酶活性在第60天达到峰值,而MDA和C2C浓度持续增加直至实验期结束。MDA和C2C浓度之间存在显著正相关,但过氧化氢酶活性与MDA或C2C浓度之间无相关性。
结果支持基于Pond-Nuki模型的氧化应激参与犬OA发病机制的假说。MDA和C2C浓度之间的相关性表明氧化应激与软骨退变之间可能存在关联。