• salecan;
  • CCl4;
  • hepatic acute injury;
  • oxidative stress;
  • hepatocyte proliferation


Carbon tetrachloride (CCl4) is a well-established model for screening hepato-protective drugs. The aim of the present study was to evaluate the potential protective effects of a novel soluble β-glucan salecan on acute liver injury induced by CCl4 in mice and to further explore the underlying mechanisms. Mice were given salecan (40 mg kg−1) or phosphate-buffered saline for 3 days prior to treatment with a single intraperitoneal dose of CCl4 (1 ml kg−1 body weight). Animals were sacrificed at 0, 12, 24, 48, 72 and 96 h post-injection of CCl4. 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 CCl4 intoxication and liver recovery was markedly accelerated at a later stage in salecan pre-administered mice. Furthermore, salecan administration remarkably alleviated lipid peroxidation and restored GSH depletion. Meanwhile, the expression of antioxidant genes was significantly elevated in the salecan-treated group. Interestingly, the administration of salecan remarkably enhanced hepatocyte proliferation in the recovery phase after CCl4 injection. Taken together, these results demonstrated that salecan exhibits a protective action on acute hepatic injury induced by CCl4 through attenuating oxidative stress and accelerating hepatocyte regeneration. Copyright © 2011 John Wiley & Sons, Ltd.