Oxidant damage in Kashin-Beck disease and a rat Kashin-Beck disease model by employing T-2 toxin treatment under selenium deficient conditions
Oxidant damage in Kashin-Beck disease and a rat Kashin-Beck disease model by employing T-2 toxin treatment under selenium deficient conditions
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DOI：
10.1002/jor.22073
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发表时间：
2012-08-01
影响因子：
2.8
通讯作者：
Chen, Chen
中科院分区：
文献类型：
--
作者：
Chen, Jing-hong;Xue, Senghai;Chen, Chen
大骨节病（KBD）是一种地方性退行性骨关节病，但其发病机制尚不清楚。这项研究使用一种新模型比较了抗氧化能力和脂质过氧化，其中大鼠在暴露于 T-2 毒素 4 周之前先接受缺硒饮食 4 周。在缺硒饮食加T-2毒素治疗的大鼠中，观察到表明细胞死亡的细胞形态和空软骨细胞腔隙的变化，以及膝关节软骨深部的软骨蛋白聚糖损失。这些变化与之前在大骨节病中观察到的变化相似。与正常饮食组相比，所有实验组中指示血清和软骨中脂质过氧化的硫代巴比妥酸反应物质（TBARS）水平均显着增加，而以总抗氧化能力（T-AOC）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPX）衡量的抗氧化剂水平在 血清和软骨均显着低于正常饮食组。单独使用 T-2 毒素或缺硒饮食加 T-2 毒素治疗可显着降低软骨组织中这些抗氧化剂的 mRNA 表达。这些结果表明，在缺硒的营养状况下，通过 T-2 毒素治疗，增加 TBARS 并减少血清和软骨中的抗氧化剂，可能会改变关节组织的氧化应激，并促进大骨节病软骨损伤的病理过程。 (C) 2012 年骨科研究学会。出版者：Wiley periodicals, Inc. J Orthop Res 30:12291237, 2012
Kashin-Beck disease (KBD) is an endemic degenerative osteoarthropathy, but the mechanisms underlying its pathogenesis remains unclear. This study compares antioxidant capacity and lipid peroxidation using a novel model, in which rats were administered a selenium-deficient diet for 4 weeks prior to their exposure to T-2 toxin for 4 weeks. Changes in cell morphology and empty chondrocyte lacunae indicative of cell death, as well as cartilage proteoglycan loss in the deep zone of articular cartilage of knee joints were observed in rats with selenium-deficient diet plus T-2 toxin treatment. These changes were similar to those observed previously in KBD. The levels of thiobarbituric acid reactive substances (TBARS), indicative of lipid peroxidation in serum and cartilage, were significantly increased in all experimental groups compared to the normal diet group, while the levels of antioxidants, measured as total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidases (GPX), in serum and cartilage were significantly lower than that in the normal diet group. The mRNA expression of those antioxidants in cartilage tissue was significantly reduced by T-2 toxin alone or by selenium-deficient diet plus T-2 toxin treatment. These results indicate that increasing TBARS and decreasing antioxidants in serum and cartilage by T-2 toxin treatment with a selenium-deficient nutritional status may alter oxidative stress in joint tissues and contribute to the pathological process of cartilage damage in KBD. (C) 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:12291237, 2012