Protective effects of an acidic polysaccharide isolated from fruiting bodies of Ganoderma lucidum against murine hepatic injury induced by Propionibacterium acnes and lipopolysaccharide

Fruiting bodies of Ganoderma lucidum were extracted with chloroform followed by hot water, from which an acidic polysaccharide named GLAa was separated and purified using 10% CCl₃COOH followed by column chromatography on DE-52 cellulose and Toyopearl HW-65. Chemical and spectroscopic analyses showed that GLAa was composed of Glc, Gal, Man and Fuc (1:0.013:0.009:0.024), in which β-d-(1→6)-Glc, β-d-(1→3)-Glc and β-d-(1→4)-Glc linkages comprised 34.9, 33.9, and 28.7% of the total linkages, respectively. The average molecular weight of GLAa was 12.5×10⁵ Da and the optical rotation was [a]^{25° textC}_textD = - 9.1^° [alpha ]^{{25^circ {text{C}}}}_{{text{D}}} = - 9.1^circ ; c =0.55, H₂O. Uronic (mannuronic) acid accounted for 14.8% of the molecule, protein, 0.14% and nitrogen, 0.75%. The hepatoprotective effect of GLAa was evaluated using a mouse model in which hepatic injury was induced with Propionibacterium acnes and lipopolysaccharide (LPS). GLAa (0.4 and 0.8 g kg⁻¹ day⁻¹, b.w., p.o.), significantly prevented increases in serum aspartate aminotransferase and alanine aminotransferase levels in mice exposed to P. acnes–LPS, indicating that GLAa has hepatoprotective activity in vivo.