日本刺参酸性粘多糖、皂苷和胶原蛋白多肽对血管内皮细胞的保护作用

Protective effects of polysaccharides,triterpene glycosides and collagen polypeptides from Apostichopus japonicus on vascular endothelial cells

目的研究日本刺参酸性粘多糖、皂苷和胶原多肽对血管内皮细胞的保护作用。方法采用ox-LDL建立体外培养的人脐静脉血管内皮细胞株(ECV304)损伤模型。MTT法测定血管内皮细胞的增殖活性;硝酸还原酶法测定血管内皮细胞一氧化氮合酶(NOS)活力和NO释放量;TBA法测定细胞内MDA含量;DNA-Ladder法检测血管内皮细胞的凋亡。结果不同浓度的酸性粘多糖、胶原蛋白多肽和低浓度的皂苷能明显抑制ox-LDL对血管内皮细胞的损伤,促进血管内皮细胞增殖(P<0.05,P<0.01);降低细胞内MDA含量(P<0.05,P<0.01);拮抗ox-LDL引起的血管内皮细胞凋亡。酸性粘多糖和胶原蛋白多肽还能明显促进血管内皮细胞NO释放量(P<0.05,P<0.01),提高细胞NOS活力(P<0.05,P<0.01)。结论日本刺参酸性粘多糖、皂苷和胶原蛋白多肽对血管内皮细胞的脂质过氧化物损伤均具有明显的保护作用。

Aim To investigate the protective effects of polysaccharides, triterpene glycosides and collagen polypeptides from Apostichopus japonicus on vascular endothellial cells damaged by ox-LDL. Methods Human umbilical yein endothelial cells （ ECV304 ）cell had been cultured in vitro, and we established an model of endothelial cell oxidative damage induced by oxidized low density lipoprotein （ox-LDL）. MTT assay was used to test the influence of polysaccharides, triterpene glycosides and collagen polypeptides from Apostichopus japonicus on proliferation activities of endothelial cells. The influence on contents of MDA was examined by TBA assay. Nitric acid deoxidize enzyme assay was used to observe the influence on the contents of NO and activities of NOS. Apoptosis of vascular endothellial cells was measured by DNA-ladder. Results All concentrations of polysaccharides, collagen poly-peptide and low concentration of triterpene glycosides could protect vascular endothellial cells from injury induced by ox-LDL. Cell proliferation activities, the contents of MDA were decreased remarkably （P 〈 0. 05, P 〈0. 01 ）, and cell apoptosis induced by ox-LDL was inhibited observably （ P 〈 0. 05, P 〈 0. 01 ）. Meanwhile, NO contents and NOS activities were stimulated significantly by polysaccharides and collagen polypeptide （P 〈 0. 05, P 〈 0. 01 ）, Conclusion Polysaccharides, triterpene glycosides and collagen polypeptides from Apostichopus japonicus have the protective effects on vascular endothelial cells oxidative damaged by ox- LDL.