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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
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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.
出处 《中国地方病防治》 北大核心 1996年第1期1-4,共4页 Chinese Journal of Control of Endemic Diseases
关键词 软骨型蛋白多糖 肥大软骨细胞 白细胞介素-1 Interleuk in-1β Proteoglycan Hypertrophic chondrocyte
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