Separation and physicochemical properties of polysaccharides from Morinda officinalis and their effects on human liver cells / 国际药学研究杂志

ABSTRACT

Objective: To separate the fractions and components of crud polysaccharides MOP-60 and MOP-60-100 from Morinda officinalis, characterize their physicochemical properties and effects on the LO2 cell proliferation as well as on the ConA- and H2O2-induced LO2 cell death. Methods: The five fractions(MOP-60-A, MOP-60-B, MOP-60-100-A, MOP-60-100-B and MOP-60- 100-C)were obtained by column chromatographic separation of MOP-60 or MOP-60-100 on a DEAE-DEAE-cellulose column. A component MOP-60-Ⅰ was obtained by dialysis of MOP-60-A. The further separation and purification of MOP-60-100-B by the Sephadex G-100 column chromatography afforded the other two components MOP-60-100-Ⅰ and MOP-60-100-Ⅱ. The molecular distribution was determined with gel filtration chromatography. The monosaccharide compositions were analyzed with capillary electrophoresis after acid hydrolysis and PMP derivation. The effects of the fractions and components of polysaccharides on the human LO2 liver cell proliferation and on the ConA- and H2O2-induced LO2 cell damage were evaluated by the MTT method. Results: MOP-60-A, MOP-60-100-A and MOP-60-Ⅰ were composed of fructose(fructosan), and the peak relative molecular mass of MOP-60-Ⅰ was 2339. MOP-60-B, MOP-60-100-B, MOP-60-100-C, MOP-60-100-Ⅰ and MOP-60-100-Ⅱ were composed of multiple monosaccharides and heteroglycans. The peak relative molecular mass of MOP-60-100-Ⅰ and MOP-60-100-Ⅱ were 62 828 and 7783, respectively. MOP-60-B, MOP-60-100-B and MOP-60-100-C increased human LO2 hepatocyte proliferation and reduced the ConA-induced LO2 cell death at 250 mg/L(P<0.01, compared to solvent or ConA alone group). MOP-60-100-C also reduced the H2O2-induced LO2 cell death at 100 and 250 mg/L(P<0.05 and P<0.01, compared to H2O2 alone group). Conclusion: The acidic fractions MOP-60-100-B and MOP- 60-100-C from M. officinalis significantly promoted LO2 cell proliferation and inhibited the ConA- and H2O2-induced cell damage in human liver LO2 cells.