目的建立低硒饲料与T-2毒素染毒致SD大鼠的大骨节病动物模型。方法断乳SD大鼠随机分为常规饲料组和低硒饲料组,饲养1个月,全血硒和血清GSH-Px测定,确定大鼠处于低硒状态后,再将大鼠随机分为6组,T-2毒素灌胃饲养1个月后处死,进行常规HE染色,光镜下观察大鼠膝关节软骨病理改变。结果在低硒饲料加低T-2毒素组和低硒饲料加高T-2毒素组,部分病例可见在骨质交界处的软骨组织深层有片状坏死,软骨细胞死亡变为红染的"细胞影子",或红染的无结构区域;以及软骨的营养不良性变化,如"原纤维显现"、波纹状钙化线和横骨梁形成等。结论本结果为低硒条件下T-2毒素在大骨节病病因中的作用提供了实验依据。
Objective To establish the Kaschin-Beck Disease rat model with T-2 toxin and the low selenium deficiency conditions.Methods One hundred and forty Sprague-Dawley(SD) rats(all male) weighing 60~80 g were randomly divided into two groups,which were fed for four weeks with AIN93 diet and selenium-deficient AIN93 diet,respectively.After the low-selenium status of rats were determined through examining blood selenium and serum GSH-Px activity level in the rats,they were randomly divided into six groups,which were fed with 100 ng/g·BW /d T-2 toxin alone or plus selenium-deficient AIN93 diet and 200 ng/g·BW /d T-2 toxin alone or plus selenium-deficient AIN93 diet and their control group respectively.Knee joint cartilage of rat were examined pathologically for occurrence of chondronecrosis microscopically.Results Chondronecrosis in deep zone of articular cartilage of knee joint were seen in both the 100 ng/g·BW /d T-2 toxin plus selenium-deficient AIN93 diet and 200 ng/g·BW /d T-2 toxin plus selenium-deficient AIN93 diet group,and chondronecrotic lesion in the two groups of rats were similar to the chondronecrotic lesion of articular cartilage in human KBD.Chondronecrosis could be seen in epiphyseal growth plate in human KBD but this could not be seen in the present study.Conclusions Both T-2 toxin and selenium deficient condition are maybe the etiology factor for KBD.