中文摘要：

目的观察实验性大鼠关节软骨损伤时血清中“型胶原降解产物”型胶原羧基端端肽（CTX-Ⅱ）和脱氧吡啶啉（DPD）水平，探讨其在软骨损伤中的分子生物标志物作用。方法利用大鼠，进行亚慢性毒性试验，通过透明软骨的组织病理和超微结构改变来确定软骨的损伤程度，用ELBA夹心法检测大鼠不同阶段血清CTX—Ⅱ和DPD含量。结果T-2毒素可致大鼠关节软骨细胞变性，坏死，出现大面积无细胞区，胶原染色可见明显的“胶原显现”；扫描电镜显示，关节面起伏不平，表面粗糙，胶原纤维断裂、剥脱，关节表面布满裂片状凸起，呈典型的关节“干燥”现象；ELBA检测结果表明，T-2毒素组大鼠血清CTX—Ⅱ水平在3个月时较对照组明显增加，差异具有统计学意义。至6个月时，CTX-Ⅱ含量虽较对照组高，但差异无统计学意义；DPD检测结果正好相反，5个月时两组无差异，6个月时T-2毒素组较对照组明显升高，差异有统计学意义。结论血清CTX—Ⅱ和DPD可作为关节软骨损伤的生物标志，但两指标反映的病理阶段不同，CTX-Ⅱ在关节软骨损伤早期反应敏感，可作为早期生物标志物，而DPD在软骨损伤后期更敏感，可作为病情进展的生物标志物。

英文摘要：

Objective To investigate the level of CTX-Ⅱ and deoxypyridinoline （DPD） in serum of experimental rats induced by T-2 toxin, to explore its roles as the biomarker of articular cartilage damage. Methods A subchronic test on rats was carried out, and to make sure the damage degree by observing the histopathological and ultrastructural changes of transparent cartilage. At the same time, the content of CTX-Ⅱ and PDP in rat serum at different experimental stage was determined by ELISA kits. Results T-2 toxin could cause rat articular chondroncytes degeneration, necrosis, and appeared many blank areas free cells. Weigert/Van Gieson staining showed obvious collagen fasciculi emergence could be seen. Scanning electronic microscope showed the surface of articular cartilage was wave and rough. Collagen fasciculi ruptured and stack up, and presented a typical ＂articular dryness＂ phenomenon. ELISA results indicated, at the stage of 3 month, the level of rat serum CTX-Ⅱ in T-2 toxin group was higher than that in control group, and the difference had a markedly significance. To the stage of 6 month, the difference had no significance. In opposition, at 3 month, the level of PDP had no difference between two groups, but to the stage of 6 month, the level of PDP in T-2 toxin group was higher than that in control group, and the difference had a markedly significance. Conclusion CTX-Ⅱ and PDP in serum could be as biomarkers for articular cartilage damage, but the two markers indexed different pathological stages, namely CTX-Ⅱ was sensitive at the early stage of cartilage damage, and could be an early biomarker and PDP was sensitive at the evolving stage, and could be a progress biomarker.