The Effects Of Ginseng Pectin On Human Umbilical Endothelial Cell (HUVEC) Migration

Angiogenesis plays an important role in continuous growth and subsequent metastasis ofcancers. The migration of vascular endothelical cells (VECs) is a key factor which affects thedevelopment of angiogenesis. Recently, it has been paid more attention on the inhibitioneffects of ginseng pectins on the VECs migration. Therefore, we tested the effects of ginsengpectins on human umbilical endothelial cell (HUVEC) migration in this paper, anddemonstrated in detail how pectins inhibited the migration induced by Galectin-3(Gal-3)，Fibronectin(FN), the MDA-MB-231cell conditioned medium and HT29cell conditionedmedium, respectively.The ginseng polysaccharides we used included the neutral fraction(WGPA-UDN), thearabinogalactan AG1and AG2, HM-HG contained highly methyl-esterified HG-rich domainand four kinds of RG-I-rich pectins named RG-I-1, RG-I-2, RG-I-3B and RG-I-4, which haddifferent monosaccaride copositions. The eight kinds of ginseng polysaccharides weredifferent in structure.The results of the scratching assays showed that WGPA-UDN, AG1and AG2had noinhibition effects on HUVEC migration at0.01mg/ml to1.0mg/ml, when thechemoattractants were Gal-3, FN, the MDA-MB-231and HT29cell conditioned mediums,respectively. However, HM-HG, RG-I-1, RG-I-2, RG-I-3B and RG-I-4inhibited the cellmigration more significantly, and the effects were dose-dependent, represented mostsignificantly when the chemoattractant was Gal-3. When the chemoattractant was Gal-3, theinhibitions of the five kinds pectins were the strongest, and the relative inhibition of RG-I-4could reach40%at1.0mg/ml. The inhibition effect of HM-HG on cell migration mediated byGalectin-3was smaller than the effects of the pectins contained RG-I domain. By contrast, thefive kinds pectins inhibited the migration similarly when Gal-3was not the chemoattractant.If the chemoattractant and the concentration of pectins were same, the effects of RG-I-1,RG-I-2, RG-I-3B and RG-I-4differed little, although they had different structures.To further verify the above findings, transwell assays were employed to check theinhibition effects of pectins. The results were similar to the scratching assay. When Gal-3, FN,the MDA-MB-231and HT29cell conditioned mediums were chemoattractants, WGPA-UDN,AG1and AG2did not inhibit the migration of HUVEC. However, the other pectins, HM-HG,RG-I-1, RG-I-, RG-I-3B and RG-I-4had more significant inhibitions on HUVEC migration,revealed dose-dependent. When the chemoattractant was Galectin-3, the effects of RG-I-1,RG-I-2, RG-I-3B and RG-I-4were stronger than HM-HG. In other conditions, the effects of HG-and RG-I-rich pectins were similar. HUVEC migration induced by Galectin-3wasinhibited most significantly by pectins, the relative migration was reduced to35%by RG-I-4at1.0mg/ml. When the chemoattractant was FN, the relative inhibition was only20%at1.0mg/ml.Considering the structural features related to the inhibitory effects, we believed that theinhibitory effects of different kinds of pectins were closely related to the GalA content andthe RG-I domain. RG-I-rich pectins contained GalA and RG-I domain, exerted stronger effectthan HG-rich pectin. The inhibition effects of ginseng pectins were probably mediatedthrough binding the chemoattractant directly.These findings represent a significant contribution towards understanding the anti-tumoractivities of ginseng pectins and supply us a new way to treat cancer.