人参多糖抗大鼠骨关节炎及其机制研究

Effects and mechanism of Giseng polysaccharides on rats'osteoarthritis

目的:研究人参多糖抗大鼠骨关节炎的作用。方法:大鼠膝关节4%木瓜蛋白酶骨关节炎造模后用不同浓度(0.1,0.25,0.5μg/ml)人参多糖行关节腔注射,作软骨组织学观察,检测血液、滑膜超氧化物歧化酶活性、丙二醛与糖胺多糖含量。分离大鼠关节软骨细胞传代培养并加入10 ng/ml白介素-1β造模,加入不同浓度(0.1,1,10,100 ng/ml)人参多糖,48 h后检测细胞增殖、糖胺多糖含量、葡萄糖醛酸转移酶ⅠmRNA表达及透射电镜细胞形态学观察。结果:人参多糖可减轻关节软骨的退变,降低血清、滑膜的丙二醛水平,增加超氧化物歧化酶活性,增加软骨中糖胺多糖含量。人参多糖对大鼠软骨细胞增值率无影响;10 ng/ml、100 ng/ml的人参多糖可以增加软骨细胞内糖胺多糖的合成;100 ng/ml的人参多糖能增加葡萄糖醛酸转移酶ⅠmRNA的表达。结论:人参多糖通过促进关键酶葡萄糖醛酸转移酶Ⅰ的表达增加糖胺多糖合成以及抗氧化作用抑制其降解来发挥对大鼠骨关节炎的治疗作用。

Objective：To investigate the effects and mechanism of Giseng polysaccharides （ GPS） on rat osteoarthritis. Methods： ①The rats began to receive GPS of 0. 1,0. 25,0. 5 μg/ml injecting after the rat models of osteoarthritis were established by intra-ariticular injection of 4 % papain. Macroscopic and histological analysis were performed on the articular cartilage; the activity of SOD,the contents of MDA in the serum and synovium and the contents of glycosaminoglycan （GAG） in the articular cartilage were detected. ②Chondrocytes isolated from rat＇s knee and shoulder joint cartilage were cultured and passaged. After monolayers were established,chondrocytes induced by 10 ng/ml IL-1β were treated with GPS of 0. 1,1,10,100 ng/ml respectively for 48h. The effects on chondrocytes were analyzed using MTT assay for chondrocyte proliferation and 1,9-dimethylmethylene blue assay for GAG content. mRNA expression of galactose-β-1,3-glucurono-syltransferaseⅠ （GlcAT-1） by rat chondrocytes was analyzed using a RT-PCR. Results： ①GPS could significantly repair cartilage degeneration、reduce the levels of MDA、enhance the SOD activity and increase the levels of GAG in the articular cartilage （P 0. 05） . ②GPS had no toxic or proliferating effect on chondrocytes in all observed concentrations. GPS of 10 ng/ml,100 ng/ml up-regulated GAG synthesis （P 0. 01） ; GPS of 100 ng/ml enhanced the expression of GlcAT-1. Conclusion： GPS have therapeutic effects on rats osteoarthritis by enhancing the expression of GlcAT-1 and antioxidant effect to increase GAG synthesis and inhibit its degradation .