title: Protective effects of salecan against carbon tetrachloride-induced acute liver injury in mice.
abstract: 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.
authors: Center for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, 210094, China.
authors: Peng
authors: P
authors: Chen
authors: Zhongqiu
authors: Z
authors: Wang
authors: Liyan
authors: L
authors: Zeng
authors: Shiming
authors: S
authors: Wang
authors: Wei
authors: W
authors: Dong
authors: Aiqun
authors: A
authors: Jia
authors: Chun
authors: C
authors: Cai
authors: Jianfa
authors: J
authors: Zhang
mesh_terms: D060054:Agrobacterium / Q000378:metabolism; D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000503:physiopathology*; D049109:Cell Proliferation / Q000187:drug effects; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D008115:Liver Regeneration / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009336:Necrosis; D018384:Oxidative Stress / Q000187:drug effects; D010088:Oxidoreductases / Q000378:metabolism; D011135:Polysaccharides, Bacterial / Q000737:chemistry / Q000302:isolation & purification / Q000378:metabolism / Q000627:therapeutic use*; D020011:Protective Agents / Q000737:chemistry / Q000302:isolation & purification / Q000378:metabolism / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D012995:Solubility; D047071:beta-Glucans / Q000737:chemistry / Q000302:isolation & purification / Q000378:metabolism / Q000627:therapeutic use*
chemical_list: D011135:Polysaccharides, Bacterial; D020011:Protective Agents; D012333:RNA, Messenger; D047071:beta-Glucans; C577623:salecan; D010088:Oxidoreductases; D005978:Glutathione