The Effect of Disordered Glycometabolism of Kashin-Beck Disease on the Function of Chondrocytes

Objective To reveal the effect of disordered glycometabolism in Kashin-Beck disease (KBD) chondrocytes, we compared changes in expressions of extracellular matrix components (collagen and aggrecan), apoptosis and oxidative stress under the condition of different concentrations of glucose. Methods The damage of KBD chondrocytes and normal chondrocytes under high glucose culture was measured in compared with cells under normal culture, that included the changes of proliferation and morphology; the concentrations of glucose in culture medium during the process of chondrocytes culture; the expressions of type Ⅱ collagen and aggrecan detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Toluidine blue staining; cell apoptosis and reactive oxygen species (ROS) content detected by flow cytometry and fluorescence staining. Results The growth and proliferation of KBD chondrocytes were inferior to normal chondrocytes. The glucose uptake of KBD chondrocytes and normal chondrocytes under high glucose culture were basically the same (P>0.05). Disordered glycometabolism caused by high glucose decreased the expression of type Ⅱ collagen and aggrecan in KBD chondrocytes (P<0.05), meanwhile, increased apoptosis and cellular ROS generation of cultured chondrocytes (P<0.05). Conclusion The disordered glycometabolism can affect the function of KBD chondrocytes through reducing the expression of type Ⅱ collagen and aggrecan and increasing the apoptosis and the oxidative stress.