Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin-Beck disease using T-2 toxin and selenium deficiency conditions
Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin-Beck disease using T-2 toxin and selenium deficiency conditions
复制标题
DOI：
10.1007/s00296-011-2335-7
复制
发表时间：
2013-01-01
影响因子：
4
通讯作者：
Hughes, Clare
中科院分区：
文献类型：
--
作者：
Guan, Fang;Li, Siyuan;Hughes, Clare
本研究旨在观察T-2毒素对缺硒营养状态下大鼠关节软骨的致病性损害，以探讨大骨节病（KBD）的可能致病因素。Sprague-Dawley大鼠在暴露于T-2毒素前4周喂食缺硒或对照饮食。在4周后形成六个饮食组并进行研究，即，对照组、缺硒组、低T-2毒素组、高T-2毒素组、缺硒饮食加低T-2毒素组、缺硒饮食加高T-2毒素组。通过测定谷胱甘肽过氧化物酶活性和血清硒水平证实硒缺乏。光镜下观察实验大鼠膝关节软骨的形态和病理变化，组织化学染色检测蛋白多糖的表达。低、高T-2毒素加低硒饮食组的膝关节软骨深层均出现软骨坏死，与人大骨节病软骨坏死十分相似。然而，在单独用T-2毒素或T-2毒素加硒饮食处理的动物的大鼠骨骺生长板中观察到的软骨坏死与在人类大骨节病中发现的软骨坏死不同。我们的研究结果表明，大鼠可以作为一个合适的动物模型，用于研究致病因素的发病机制（软骨坏死）在人类大骨节病观察。然而，在骨骺生长板中观察到的这些变化与在人类大骨节病中观察到的变化不同，这可能是因为在大鼠中没有生长板闭合。
The objective of this study is to observe pathogenic lesions of joint cartilages in rats fed with T-2 toxin under a selenium deficiency nutrition status in order to determine possible etiological factors causing Kashin-Beck disease (KBD). Sprague-Dawley rats were fed selenium-deficient or control diets for 4 weeks prior to their being exposed to T-2 toxin. Six dietary groups were formed and studied 4 weeks later, i.e., controls, selenium-deficient, low T-2 toxin, high T-2 toxin, selenium-deficient diet plus low T-2 toxin, and selenium-deficient diet plus high T-2 toxin. Selenium deficiencies were confirmed by the determination of glutathione peroxidase activity and selenium levels in serum. The morphology and pathology (chondronecrosis) of knee joint cartilage of experimental rats were observed using light microscopy and the expression of proteoglycans was determined by histochemical staining. Chondronecrosis in deep zone of articular cartilage of knee joints was seen in both the low and high T-2 toxin plus selenium-deficient diet groups, these chondronecrotic lesions being very similar to chondronecrosis observed in human KBD. However, the chondronecrosis observed in the rat epiphyseal growth plates of animals treated with T-2 toxin alone or T-2 toxin plus selenium-deficient diets were not similar to that found in human KBD. Our results indicate that the rat can be used as a suitable animal model for studying etiological factors contributing to the pathogenesis (chondronecrosis) observed in human KBD. However, those changes seen in epiphyseal growth plate differ from those seen in human KBD probably because of the absence of growth plate closure in the rat.