雪腐镰刀菌烯醇和硒对培养软骨组织CD44表达的影响

Study of adhesion molecule CD44 on the effect of nivalenol and the protective effect of selenium on the reestablished human cartilage in vitro

目的 研究大骨节病(KBD)有关病因因素对靶组织细胞的损伤和保护作用;探索引起软骨细胞变性坏死的机制。方法 采用细胞培养法于体外再建软骨组织模型,并加入KBD可疑致病因子雪腐镰刀菌烯醇(NIV)和保护因子硒,检测软骨细胞膜上透明质酸受体CD44和细胞培养液中可溶性CD44(SoCD44)。结果 软骨细胞膜上CD44的表达随着,NIV浓度的增加而减少,加硒后有增加趋势;细胞培养液中SoCD44浓度随NIV浓度升高逐渐降低,但高浓度组出现了增高,加硒后趋势不变;除对照组与加硒对照组外,组间差异有统计学意义(P<0.05)。结论 NIV能干扰软骨细胞表面粘附分子CD44表达,进而引起软骨细胞外基质代谢紊乱;补硒能够拮抗NIV对软骨细胞的损伤,但作用有限。

Objective To investigate the mechanisms of NIV and Se in the process of Kaschin Beck disease (KBD). Methods We detected the CD44 on the cartilage chondrocyte cultured in vitro and soluble CD44 in the culture medium. Results The expression of CD44 on chondrocyte decreased with the increasing of the concentration of NIV in medium, and Se could increase the expression of CD44 on chondrocyte. The SoCD44 in medium decreased with the increasing of the concentration of NIV, but there was an exception in high concentration of NIV (P < 0.05). Conclusions NIV can decrease the expression of CD44 on the cartilage chondrocyte and cause metabolism disorder of cartilage matrix. Se can protect chondrocyte and decrease the cartilage damaged by NIV.