白细胞介素—1促进肥大软骨细胞PG的分解代谢  

EFFECT OF INTERLEUKIN -IBON DEGRADATION OF PROTEOGLYCAN IN RABBIT HYPERTROPHIC CHONDROCYTE CULTURES

作　　者：颜炜群[1] 宇莉[1] 侯宜[1] 姜金兰[1] 杨春伟[1] 侯立中[1] 杨同书[1] 申鸣[2] 宋国培[2] 加藤幸夫 中村茂夫 

机构地区：[1]白求恩医科大学应用基础医学研究所 [2]白求恩医科大学第一临床医院内科 [3]日本广岛大学齿学部生物化学教研室

出　　处：《中国地方病防治》1996年第1期1-4,共4页Chinese Journal of Control of Endemic Diseases

摘　　要：本文观察了白细胞介素—1(IL—1β)和硫代腺苷蛋氨酸(SAM)对培养的肥大软骨细胞蛋白多糖(PG)分解代谢及基质金属蛋白水解酶(MMP)活性的影响。IL—1β(0.1—1ng/ml)能够明显促进培养的肥大软骨细胞PG分解,释放到培养液中的PG其分子量明显降低,缺乏透明质酸结合区。IL—1β(0.3ng/ml)添加组软骨细胞其MMP活性显著高于对照组;SAM具有轻微抑制IL—1促进PG分解的作用。这些结果显示了IL—1β是调节肥大软骨细胞生理和病理过程的重要的细胞因子。Effect of interleukin-1 (IL-1β) on degradation of proteoglycan and metalloproteinase (MMP) activity in rabbit hypertrophic chondrocyte cultures was examined. IL-1β(0. 01-1ng/ml) increased,in dose dependant ,release of proteoglycan from cell layer to the medium(P<0. 01). The proteoglycan released to the medium exhibited a decrease in molecular size,and ability of proteoglycan associated hyaluronic acid,when compared to control cultures.MMP activity in the medium of culture treated with IL-1β(0. 3ng/ml) remarkably increased (P <0. 01). The proteoglycan degradation caused by IL-1β was partly inhibited by S-adenosyl-L-methionine (SAM). These results suggest that JL-1β play important regulation roles in physiological or pathological growth plate chondrocyte.

关 键 词：软骨型蛋白多糖 肥大软骨细胞 白细胞介素-1 

分 类 号：R336[医药卫生—人体生理学] R361.3[医药卫生—基础医学]