人参多糖、黄芪多糖对大鼠骨关节炎细胞模型葡糖氨基聚糖合成的影响及其可能机制

Effect and mechanism of panaxan and astragalus polysaccharides on glycosaminoglycan synthesis of rat osteoarthritic chondrocytes in vitro

目的研究人参多糖(panaxan)、黄芪多糖(astragalus polysaccharides,AP)对大鼠退变软骨细胞葡糖氨基聚糖(glycosaminoglycan,GAG)合成的影响及其可能的作用机制。方法 7只Wistar大鼠(SPF级),分离提取其软骨细胞,分为空白对照组、IL-1β对照组、阳性对照组、人参多糖低、中、高和极高剂量组、黄芪多糖低、中、高和极高剂量组。倒置显微镜下观察细胞形态学变化,检测并比较各组细胞增殖情况、细胞内GAG含量、细胞内葡萄糖醛酸转移酶Ⅰ(galactose-β-1,3-glucuronosyltransferaseⅠ,Glc AT-1)mRNA含量。结果人参多糖各及黄芪多糖浓度组对大鼠软骨细胞的增殖无明显影响。但0.01、0.1 mg/L浓度的人参多糖和100 mg/L的黄芪多糖可显著促进软骨细胞内GAG的合成(均P<0.01);0.1 mg/L浓度的人参多糖和1、10、100 mg/L的黄芪多糖能够显著增加Glc AT-1 mRNA的表达(P<0.05)。结论人参多糖、黄芪多糖的主要作用是对经IL-1β作用后,并进行体外培养的大鼠软骨细胞中GAG的合成产生抑制作用,其可能的机制之一是通过促进Glc AT-1的表达来实现的。

Objective To study the effect of ginseng polysaccharides(panaxan),astragalus polysaccharide(astragalus polysaccharides,AP) on the synthesis of glycosaminoglycan(glycosaminoglycan,GAG) of cartilage cells of degeneration in rats and its possible mechanism. Methods Cartilage cells of 7 Wistar rats(SPF) were separated and extracted,then divided into seven groups: blank control group,IL-1β control group,positive control group,astragalus polysaccharides group of low,medium,high and very high dose and ginseng polysaccharides of low,medium,high and very high dose. Morphological changes of cells were observed under inverted microscope. Proliferation,GAG content,intracellular glucose transferase(galactosebeta 1,3-glucuronosyltransferase Ⅰ,Glc AT-1) mRNA levels were detected and compared. Results The ginseng polysaccharides group and astragalus polysaccharides group of different concentrations had no effect on cell proliferation rate of rat cartilage cells. 0. 01 mg / L,0. 1 mg / L of ginseng polysaccharides and 100 mg / L of astragalus polysaccharide could increase GAG synthesis of cartilage cells(both P < 0. 01); 0. 1 mg / L of ginseng polysaccharides and 1,10,100 mg / L astragalus polysaccharide could significantly increase the expression of Glc AT-1mRNA's. Conclusion Ginseng polysaccharides and astragalus polysaccharides could inhibited the GAG synthesis of rats cartilage cells treated by IL-1β in vivo. Promoting the expression of Glc AT-1 is one of its possible mechanism.