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The aim of the present study was to evaluate the potential protective effects of a novel soluble <jats:italic>\u03b2<\/jats:italic>\u2010glucan salecan on acute liver injury induced by CCl<jats:sub>4<\/jats:sub> in mice and to further explore the underlying mechanisms. Mice were given salecan (40\u2009mg kg<jats:sup>\u22121<\/jats:sup>) or phosphate\u2010buffered saline for 3\u2009days prior to treatment with a single intraperitoneal dose of CCl<jats:sub>4<\/jats:sub> (1\u2009ml kg<jats:sup>\u22121<\/jats:sup> body weight). Animals were sacrificed at 0, 12, 24, 48, 72 and 96\u2009h post\u2010injection of CCl<jats:sub>4<\/jats:sub>. Serum liver enzyme levels, histology, lipid peroxidation, glutathione (GSH) content, expression of antioxidant enzymes and hepatocyte proliferation were subsequently evaluated. The serum levels of hepatic enzyme markers were markedly reduced in the salecan pretreatment group compared with the control group. Histopathological examination of the livers revealed that hepatocellular degeneration and necrosis were significantly attenuated at an early stage during CCl<jats:sub>4<\/jats:sub> intoxication and liver recovery was markedly accelerated at a later stage in salecan pre\u2010administered mice. Furthermore, salecan administration remarkably alleviated lipid peroxidation and restored GSH depletion. Meanwhile, the expression of antioxidant genes was significantly elevated in the salecan\u2010treated group. Interestingly, the administration of salecan remarkably enhanced hepatocyte proliferation in the recovery phase after CCl<jats:sub>4<\/jats:sub> injection. Taken together, these results demonstrated that salecan exhibits a protective action on acute hepatic injury induced by CCl<jats:sub>4<\/jats:sub> through attenuating oxidative stress and accelerating hepatocyte regeneration. 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