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萨如拉, 王丽华. Ⅱ型胶原对T-2毒素诱导关节软骨损伤拮抗作用[J]. 中国公共卫生, 2015, 31(5): 603-605. DOI: 10.11847/zgggws2015-31-05-18
引用本文: 萨如拉, 王丽华. Ⅱ型胶原对T-2毒素诱导关节软骨损伤拮抗作用[J]. 中国公共卫生, 2015, 31(5): 603-605. DOI: 10.11847/zgggws2015-31-05-18
Sarula, WANG Li-hua. Protective effect of collagen-Ⅱ on articular cartilage damage induced by T-2 toxin in rats[J]. Chinese Journal of Public Health, 2015, 31(5): 603-605. DOI: 10.11847/zgggws2015-31-05-18
Citation: Sarula, WANG Li-hua. Protective effect of collagen-Ⅱ on articular cartilage damage induced by T-2 toxin in rats[J]. Chinese Journal of Public Health, 2015, 31(5): 603-605. DOI: 10.11847/zgggws2015-31-05-18

Ⅱ型胶原对T-2毒素诱导关节软骨损伤拮抗作用

Protective effect of collagen-Ⅱ on articular cartilage damage induced by T-2 toxin in rats

  • 摘要: 目的观察Ⅱ型胶原干预T-2毒素诱导大鼠关节软骨早期损伤的作用, 为探讨关节软骨损伤的防治措施提供理论依据。方法Wistar 大鼠40只, 随机分为4组, 每组10只, 对照组(常规成品颗粒料), T-2毒素组(含100 ng/kg T-2毒素饲料), Ⅱ 型胶原0.5、5.0组(0.5、5.0 g/L)连续处理5个月, 光镜下观察大鼠透明软骨组织病理学改变, 用酶联免疫吸附试验检测大鼠血清 Ⅱ 型胶原羧基端端肽(CTX-Ⅱ)、软骨寡聚基质蛋白(COMP)及尿中吡啶啉(DPD)含量。结果光镜下T-2毒素组大鼠关节软骨细胞排列紊乱, 软骨细胞变形、变性, 可见大面积软骨细胞坏死, 而低、高剂量 Ⅱ 型胶原组表现为软骨表面原纤维形成, 表层软骨细胞肿胀变圆, 扁平的软骨细胞减少, 软骨细胞簇集等骨关节炎早期病理改变。对照组, T-2毒素组, 高、低剂量 Ⅱ 型胶原组大鼠血清 CTX-Ⅱ、COMP 含量分别为(25.07±9.17)、(39.17±10.49)、(28.20±9.74)、(29.73±9.32)μg/L 与(6.38±2.23)、(24.53±4.26)、(20.32±4.74)、(19.44±4.92)μg/L, 大鼠尿液DPD含量分别为(4.14±1.06)、(4.33±3.43)、(5.72±3.89)、(4.23±2.90)μg/L。与对照组比较, 模型组大鼠血清 CTX-Ⅱ、COMP 含量明显升高(均P<0.05), 大鼠尿液 DPD 含量无明显改变;与模型组比较, Ⅱ 型胶原组大鼠血清 CTX-Ⅱ、COMP 明显降低(均P<0.05), 大鼠尿液 DPD 含量无明显变化。结论Ⅱ 型胶原能拮抗T-2毒素所致软骨损伤作用, 延缓关节软骨的破坏进程, 其机制可能与降低大鼠血清中CTX-Ⅱ 及 COMP 含量有关。

     

    Abstract: ObjectiveTo observe protective effect of collagen-Ⅱ on articular cartilage damage induced by T-2 toxin in rats, and to provide a theoretical basis for the control of articular cartilage damage.MethodsForty Wistar rats were randomly divided into four groups(10 rats in each group):blank group(fed with standard rat chow),T-2-toxin exposed group(with T-2-toxin of 100 ng/kg),collagen-II exposed group(with collagen-II of 0.5 and 5.0 g/L).After the treatment of 5 months,the articular cartilage was observed with light microscope and the content of serum C-telopeptide of type Ⅱ collagen(CTX-Ⅱ) and cartilage oligomeric matrix protein(COMP) and urinary deoxypyridinoline(DPD) were determined with enzyme-linked immunosorbent assay(ELISA) kits.ResultsDisarrangement,degeneration,and necrosis of articular chondrocytes were observed in the rats of T-2-toxin exposed group; early pathological changes of osteoarthritis(fibril formation,swelling of chondrocytes on the cartilage surface,and cluster of chondrocytes) were observed in the rats of the two collagen-II exposed groups.The levels of serum CTX-Ⅱ,COMP,and urinary DPD were 25.07±9.17,6.38±2.23,and 4.14±1.06 μg/L for the blank group,39.17±10.49,24.52±4.26,and 4.33±3.43μg/L for T-2-toxin group,29.73±9.32,19.44±4.92,and 4.23±2.90μg/L for 0.5 g/L collagen-II group,and 33.20±9.74,20.32±4.74,and 5.72±3.89 μg/L for 5.0 g/L collagen-II group,repectively.Compared with the blank group, the levels of serum CTX-Ⅱ and COMP in the T-2-toxin exposed group increased markedly, with a signigicant difference(P<0.05),and the levels of urinary DPD did not increase significantly.Compared with the model group,the levels of serum CTX-Ⅱ and COMP in the two collagen-II exposed groups decreased markedly, with a signigicant difference(P<0.05),and the level of urinary DPD did not increase significantly.ConclusionCollagen-Ⅱ could effectively delay the process of articular cartilage damage induced by T-2 toxin in rats and the mechanism may be related to the reduced CTX -Ⅱ and COMP in serum.

     

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