摘要
【目的】观察压力对体外培养SD大鼠髁突软骨细胞增殖、凋亡以及合成蛋白多糖的影响,探讨压力与软骨退变之间的相互关系。【方法】在一个大气压基础上,分别对3组体外培养髁突细胞进行加压-10kPa、10kPa,20kPa(5%CO2),以未加压组作为对照,用四唑盐法(MTT法)和流式细胞技术分别检测各组标本在加压3h和加压24h后细胞增殖、凋亡的情况;应用硫酸鄄咔唑法检测各组标本在加压3h和加压24h后蛋白多糖的含量。【结果】加压3h后,各加压组与对照组相比,细胞的增殖、凋亡以及蛋白多糖含量无明显变化;加压24h后,压力值为20kPa时可以明显拟制增殖,并诱导髁突软骨细胞发生凋亡增加,蛋白多糖含量明显减少。【结论】长时间的异常压力负荷可使髁突软骨细胞增殖减缓、凋亡增加,蛋白多糖含量减少,诱发或加重关节软骨退变。
Objective] To investigate the effect of static compression on the proliferation activity, apoptosis rate, and matrix proteoglycans synthesis in cultured mandibular condylar cartilage (MCC) cells, and the relation between abnormal compression and degradation of cartilage. [Methods] MCC cells of second generation were placed into sealed containers, which were perfused with 5% CO2 to offer 10 kPa, 20 kPa, -10 kPa static compressions respectively. No mechanical loading were applied to the control group. When the mechanical loading lasted 3 hours and 24 hours, the proliferation activity and the apoptosis rate were determined by MTT method and flow cytometry respectively, the content of matrix proteoglycans were determined by sulfuric acid-carbazole colorimetry methods. [Results] When the peak stress came to 20 kPa and last more than 24 hours, it can significantly decrease proliferation activity and the synthesis of matrix proteoglycans, increase the apoptosis rate significantly. [Conclusion] Abnormal compression could induce the apoptosis of chondrocytes and reduction in the content of proteoglycans, which may trigger or deteriorate the degradation of cartilage.
出处
《中山大学学报（医学科学版）》
CAS
CSCD
北大核心
2005年第3期282-284,共3页
Journal of Sun Yat-Sen University:Medical Sciences
基金
广东省自然科学基金资助项目(C03031906)
