Chlorella vulgaris extract ameliorates carbon tetrachloride-induced acute hepatic injury in mice

被引:59
作者
Li, Li [1 ]
Li, Wei [1 ]
Kim, Yong-ho [1 ]
Lee, Yong Woo [1 ]
机构
[1] Inje Univ, Grad Sch, Dept Smart Food & Drug, Gimhea 621749, Gyeongman, South Korea
关键词
Chlorella vulgaris extract; Carbon tetrachloride; CYP2E1; Detoxification; Antioxidant; CYTOCHROME-P450; 2E1; EXPRESSION; HOT-WATER EXTRACT; HEPATOTOXICITY; ANTIOXIDANT; METABOLISM; MECHANISMS; RADICALS; INHIBITION; RESISTANCE; INFECTION;
D O I
10.1016/j.etp.2011.06.003
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
The possible protective effects of Chlorella vulgaris extract (CVE) on carbon tetrachloride (CCl4)-induced acute hepatic injury in mice and the mechanism underlying these effects was investigated. CCl4 administration caused a marked increase in the levels of serum aminotransferases, lipid peroxidation and cytochrome P450-2E1 (CYP450) expression. Also, decreased glutathione (GSH) content and activities of cellular antioxidant defense enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase and glutathione-S-transferase (GST) were found after CCl4 exposure. All of these phenotypes were markedly reversed by preadministration of the mice with CVE. In addition, CVE exhibited antioxidant effects on FeCl2-ascorbate induced lipid peroxidation in mouse liver homogenates, and on superoxide radical scavenging activity. Taken together, these results suggest that CVE produced a protective action on CCl4-induced acute hepatic injury in mice, presumably through blocking CYP-mediated CCl4 bioactivation, inducing the GSH levels, antioxidant enzyme activities and free radical scavenging effect. Therefore, CVE may be an effective hepatoprotective agent and viable candidate for treating hepatic disorders and other oxidative stress-related diseases. (C) 2011 Elsevier GmbH. All rights reserved.
引用
收藏
页码:73 / 80
页数:8
相关论文
共 54 条
[1]   Methanol potentiation of carbon tetrachloride hepatotoxicity: The central role of cytochrome P450 [J].
Allis, JW ;
Brown, BL ;
Simmons, JE ;
Hatch, GE ;
McDonald, A ;
House, DE .
TOXICOLOGY, 1996, 112 (02) :131-140
[2]  
Aniya Y, 2000, BIOL PHARM BULL, V23, P309, DOI 10.1248/bpb.23.309
[3]   Critical evaluation of the use of hydroethidine as a measure of superoxide anion radical [J].
Benov, L ;
Sztejnberg, L ;
Fridovich, I .
FREE RADICAL BIOLOGY AND MEDICINE, 1998, 25 (07) :826-831
[4]   STUDIES OF THE RELATIONSHIP BETWEEN THE CATALYTIC ACTIVITY AND BINDING OF NON-SUBSTRATE LIGANDS BY THE GLUTATHIONE S-TRANSFERASES [J].
BOYER, TD ;
VESSEY, DA ;
HOLCOMB, C ;
SALEY, N .
BIOCHEMICAL JOURNAL, 1984, 217 (01) :179-185
[5]  
BRATTIN W J, 1985, Journal of Free Radicals in Biology and Medicine, V1, P27, DOI 10.1016/0748-5514(85)90026-1
[6]   Industrial solvents and liver toxicity: Risk assessment, risk factors and mechanisms [J].
Brautbar, N ;
Williams, J .
INTERNATIONAL JOURNAL OF HYGIENE AND ENVIRONMENTAL HEALTH, 2002, 205 (06) :479-491
[7]   ROLE OF FREE-RADICALS IN TOXIC HEPATIC-INJURY .2. ARE FREE-RADICALS THE CAUSE OF TOXIN-INDUCED LIVER-INJURY [J].
BRENT, JA ;
RUMACK, BH .
JOURNAL OF TOXICOLOGY-CLINICAL TOXICOLOGY, 1993, 31 (01) :173-196
[8]   PREVENTION OF CARBON TETRACHLORIDE-INDUCED NECROSIS BY INHIBITORS OF DRUG-METABOLISM - FURTHER STUDIES ON THEIR MECHANISM OF ACTION [J].
CASTRO, JA ;
FERREYRA, EC ;
CASTRO, CRD ;
FENOS, OMD ;
SASAME, H ;
GILLETTE, JR .
BIOCHEMICAL PHARMACOLOGY, 1974, 23 (02) :295-&
[9]   ALPHA-(PHENYLSELENENYL)ACETOPHENONE DERIVATIVES WITH GLUTATHIONE PEROXIDASE-LIKE ACTIVITY - A COMPARISON WITH EBSELEN [J].
COTGREAVE, IA ;
MOLDEUS, P ;
BRATTSAND, R ;
HALLBERG, A ;
ANDERSSON, CM ;
ENGMAN, L .
BIOCHEMICAL PHARMACOLOGY, 1992, 43 (04) :793-802
[10]   VITAMIN-A POTENTIATION OF CARBON-TETRACHLORIDE HEPATOTOXICITY - ROLE OF LIVER MACROPHAGES AND ACTIVE OXYGEN SPECIES [J].
ELSISI, AED ;
EARNEST, DL ;
SIPES, IG .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1993, 119 (02) :295-301