Shao Wan-Zhen, Zhang Feng-E, Wang Sen, Guo Xiong, Wu Cui-Yan
School of Public Health,Health Science Center of Xi'an Jiaotong University;Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission of the People's Rupublic of China,Xi'an 710061,China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2018 Mar;49(2):221-225.
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.
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.
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 (>0.05). Disordered glycometabolism caused by high glucose decreased the expression of type Ⅱ collagen and aggrecan in KBD chondrocytes (<0.05),meanwhile,increased apoptosis and cellular ROS generation of cultured chondrocytes (<0.05).
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.
为揭示大骨节病（KBD）软骨细胞糖代谢紊乱的影响，我们比较了不同葡萄糖浓度条件下细胞外基质成分（胶原蛋白和聚集蛋白聚糖）表达、细胞凋亡及氧化应激的变化。
与正常培养的细胞相比，检测高糖培养条件下KBD软骨细胞和正常软骨细胞的损伤情况，包括增殖和形态的变化；软骨细胞培养过程中培养基中葡萄糖的浓度；通过定量实时聚合酶链反应（qRT-PCR）和甲苯胺蓝染色检测Ⅱ型胶原蛋白和聚集蛋白聚糖的表达；通过流式细胞术和荧光染色检测细胞凋亡和活性氧（ROS）含量。
KBD软骨细胞的生长和增殖能力低于正常软骨细胞。高糖培养条件下KBD软骨细胞和正常软骨细胞的葡萄糖摄取基本相同（>0.05）。高糖引起的糖代谢紊乱降低了KBD软骨细胞中Ⅱ型胶原蛋白和聚集蛋白聚糖的表达（<0.05），同时增加了培养软骨细胞的凋亡和细胞ROS生成（<0.05）。
糖代谢紊乱可通过降低Ⅱ型胶原蛋白和聚集蛋白聚糖的表达、增加细胞凋亡和氧化应激来影响KBD软骨细胞的功能。
