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目的:探讨人参多糖(GPS)对大鼠关节软骨细胞糖胺聚糖(GAG)合成的影响及其作用机制。方法:分离原代大鼠关节软骨细胞进行传代培养并加入白介素-1β造模,分别将2,10,50μg·ml~(-1)的人参多糖作用于该软骨细胞48 h。检测细胞增殖、GAG含量和GAG合成酶木糖基转移酶-Ⅰ(Xyl T-Ⅰ)、半乳糖基转移酶-Ⅰ(Gal T-Ⅰ)、半乳糖基转移酶-Ⅱ(Gal T-Ⅱ)和葡萄糖醛酸转移酶-Ⅰ(Glc AT-Ⅰ)mRNA的含量和基质降解酶基质金属蛋白酶-3(MMP-3)、聚集蛋白聚糖酶-1(aggrecanase-1)和聚集蛋白聚糖酶-2(aggrecanase-2)mRNA的含量。结果:各浓度人参多糖对大鼠关节软骨细胞增殖无显著影响(P>0.05);10、50μg·ml~(-1)GPS组软骨细胞GAG含量显著高于模型对照组(P<0.01);10μg·ml~(-1)GPS可增加Xyl T-ⅠmRNA的表达(P<0.05),50μg·ml~(-1)GPS可增加Xyl T-Ⅰ、Gal T-I和Gal T-Ⅱ的mRNA表达(P<0.05或P<0.01);IL-1β可显著增加软骨细胞蛋白多糖降解酶MMP-3、aggrecanase-1和aggrecanase-2的mRNA表达(P<0.05或P<0.01),GPS对蛋白多糖降解酶表达无抑制作用。结论:GPS可促进IL-1β下调的大鼠软骨细胞GAG合成,其机制可能与促进GAG合成酶表达增加而不是抑制基质降解酶表达有关。
Objective: To investigate the effect of ginseng polysaccharide (GPS) on the synthesis of GAG in rat articular chondrocytes and its mechanism. Methods: Primary rat articular chondrocytes were isolated and subcultured. Interleukin - 1β was added into the chondrocytes to induce chondrocytes proliferation. Chondrocytes were treated with 2, 10 and 50 μg · ml -1 polysaccharides for 48 h. The cell proliferation, GAG content and the activities of GAG synthase Xyl T-Ⅰ, Gal T-Ⅰ, Gal T-Ⅱ ) And glucuronosyltransferase-I (Glc AT-I) mRNA and matrix metalloproteinase-3 (MMP-3), aggrecanase-1 and aggrecanase 2 (aggrecanase-2) mRNA content. Results: Ginseng polysaccharide had no significant effect on the proliferation of articular chondrocytes (P> 0.05). The GAG content of chondrocytes in 10,50μg · ml -1 GPS group was significantly higher than that of model control group (P <0.01). GPS at 10μg · ml -1 increased the expression of Xyl T-ⅠmRNA (P <0.05), while GPS at 50μg · ml -1 increased the mRNA expression of Xyl T-Ⅰ, Gal TI and Gal T-Ⅱ P <0.05 or P <0.01). IL-1β significantly increased the expression of proteoglycan degrading enzymes MMP-3, aggrecanase-1 and aggrecanase-2 in chondrocytes (P <0.05 or P <0.01) No inhibition of enzyme expression. Conclusion: GPS can promote the GAG synthesis of rat chondrocytes down-regulated by IL-1β, which may be related to the increase of GAG synthase expression rather than the inhibition of matrix degrading enzyme expression.