title: Potential protection of vitamin C against liver-lesioned mice.
abstract: Pathologically, liver injury can result from sustained trauma to hepatocytes, including acute damage. Thus, attenuation of hepatocellular lesion may help improve liver functions. The purpose of this study was to explore the potential advantages of vitamin C (VC) intake on acutely intralesional liver in carbon tetrachloride (CCl4)-exposed mice. Here our data showed that VC supplementation contributed to ameliorated vital signs of CCl4-lesioned mice, resulting in dose-dependent reduction of hepatomegaly. VC lowered the levels of liver functional enzymes including alanine aminotransferase (ALT) and glutamic-oxaloacetic transaminase (AST) in serum, while concentration of lactic acid concentration in blood plasma was decreased. VC-administered CCl4-lesioned mice manifested increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), while the malondialdehyde (MDA) content was reduced in liver tissue. Moreover, VC consumption attenuated hepatotoxic injuries of CCl4-lesioned mice, in which the number of TNF-α positive cells was dose-dependently reduced. Furthermore, intrahepatic expression of TRL-4 mRNA, a vital inflammation-regulator, was down-regulated in VC-administered mice. Overall, we conclude that VC has the potentiality of anti-hepatotoxicity that is capable of ameliorating liver functions, speculating that therapeutic mechanism relates to normalizing metabolism and blocking inflammatory stress in the liver.
authors.affiliation: Faculty of Basic Medicine, Guilin Medical University, Guilin 541004, PR China.
authors.forename: Min
authors.initials: M
authors.lastname: Su
authors.affiliation: Department of Pathology, Guigang City People's Hospital, Guigang, Guangxi 537100, PR China.
authors.forename: Hongqiu
authors.initials: H
authors.lastname: Chen
authors.affiliation: Central Pharmacy, Guigang City People's Hospital, Guigang, Guangxi 537100, PR China.
authors.forename: Chaohe
authors.initials: C
authors.lastname: Wei
authors.affiliation: Guangxi Medical University, Nanning 530021, PR China; Guilin Medical University, Guilin 541004, PR China.
authors.forename: Ning
authors.initials: N
authors.lastname: Chen
authors.affiliation: Guilin Medical University, Guilin 541004, PR China. Electronic address: college_wuwei@126.com.
authors.forename: Wei
authors.initials: W
authors.lastname: Wu
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005979:Glutathione Peroxidase / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics
chemical_list: D020011:Protective Agents; D012333:RNA, Messenger; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D008315:Malondialdehyde; D002251:Carbon Tetrachloride; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001205:Ascorbic Acid
keywords: Hepatotoxicity; Inflammation; Metabolism; Vitamin C