Hepatoprotective effect of 2,3-dehydrosilybin on carbon tetrachloride-induced liver injury in rats

The aim of this study was to investigate the protective effect of 2,3-dehydrosilybin (DHS) against carbon tetrachloride (CCl₄)-induced liver injury in rats. Administration of DHS significantly attenuated the levels of serum aspartate aminotransferase, alanine aminotransferase, and liver lipid peroxidation in CCl₄-treated rats. Moreover, we showed that DHS prevented DNA damage and decreased the protein levels of γ-H2AX, which is a specific DNA damage marker, in CCl₄-treated rat livers. DHS also markedly increased the activity of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase in CCl₄-treated rat livers. Furthermore, we found that DHS significantly inhibited the production of serum nitric oxide as well as the levels of serum IL-6, IFN-γ, and TNF-α in CCl₄-treated rats. Additionally, DHS significantly suppressed iNOS expression on the protein levels in CCl₄-treated rat livers. Collectively, the present study suggests that DHS protects the liver from CCl₄-induced hepatic damage via antioxidant and anti-inflammatory mechanisms.     

Protective effect of antrosterol from Antrodia camphorata submerged whole broth against carbon tetrachloride-induced acute liver injury in mice

The hepatoprotective potential of antrosterol (ergostatrien-3β-ol, ST1) from Antrodia camphorata (AC) against carbon tetrachloride (CCl₄)-induced liver damage was evaluated in preventive models in mice. Pretreatment with ST1 markedly prevented the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and liver lipid peroxides in CCl₄-treated mice. The activities of antioxidant enzymes [catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)] were significantly increased after treatment with CCl₄invivo. In addition, ST1 decreased the level of nitric oxide (NO) production and tumour necrosis factor-alpha (TNF-α) in CCl₄-treated mice. In this study, these results pointed out that ST1 can inhibit lipid peroxidation, enhance the activities of antioxidant enzymes, decreases the TNF-α level, nitric oxide production and inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) expressions. Therefore, it was speculated that ST1 protects mice from liver damage through their anti-inflammation capacity.     

Hepatoprotective effect of fermented rice bran against carbon tetrachloride-induced toxicity in mice

The protective effect of fermented rice bran (GF) against carbon tetrachloride (CCl₄)-induced hepatotoxicity in mice was investigated. Hepatic fibrosis was induced via long-term oral administration of CCl₄. GF was added to feed. Mice sera were analyzed 8 weeks after administration. The alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, both markers of hepatic injury, were reduced in the GF group. Total cholesterol (TC) and triglycerides (TG) levels were also reduced. The glutathione (GSH) level, an antioxidant in liver tissue, increased. Collagen is major component of the extracellular matrix (ECM). Persistent liver damage causes excess remodeling of liver tissue and ECM deposition, causing liver fibrosis. Liver injury was reduced and the amount of collagen, which is synthesized during recovery from liver injury, was significantly reduced in GF fed mice. Thus, the liver was protected against toxic chemicals by GF in mice with CCl₄-induced hepatic fibrosis with an increased antioxidative reaction.     

Characterisation of polysaccharides from green tea of Huangshan Maofeng with antioxidant and hepatoprotective effects

This study was to examine the hepatoprotective effects of polysaccharides from green tea of Huangshan Maofeng (HMTP) against CCl₄-induced oxidative damage in mice. HMTP is an acidic heteropolysaccharide with galactose (35.0%, mol.%), arabinose (28.9%) and galacturonic acid (11.3%) being the main monosaccharide components. HMTP (400 and 800 mg/kg·bw) administered orally daily for 14 days before CCl₄ administration significantly reduced the impact of CCl₄ toxicity on the serum markers of liver damage, alanine aminotransferase, aspartate aminotransferase, total-cholesterol and triglycerides. This method of HMTP administration also markedly restrained hepatic lipid peroxidation formation of malondialdehyde and 15-F_2t isoprostanes, and elevated the antioxidant levels of hepatic glutathione and superoxide dismutase. These results together with liver histopathology indicated that HMTP exhibited hepatoprotection against CCl₄-induced injury, which was found to be comparable to that of biphenyldicarboxylate. The hepatoprotective effects of HMTP may be due to both the inhibition of lipid peroxidation and the increase of antioxidant activity.     

Hepatoprotective and antioxidant activity of anthocyanins in black rice bran on carbon tetrachloride-induced liver injury in mice

The benefits of anthocyanin-rich black rice bran extract (ARBE) on the liver of carbon tetrachloride (CCl₄)-intoxicated mice was investigated. Based on the in vivo experiment, the effect of cyanidin-3-glucoside (Cy-3-G) and peonidin-3-glucoside (Pn-3-G), the predominant anthocyanins in ARBE, on CCl₄ insulted hepatocytes L-02 was further evaluated. Mice treated with ARBE for 7 weeks by oral administration showed reduced aminotransferase activities in serum, accompanied by enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity, while tiobarbituric acid reactive substances (TBARS), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels were significantly decreased compared to CCl₄-intoxicated model group. Histopathological observation showed ARBE administration alleviated the pathological changes in livers of CCl₄-intoxicated mice. Similarly, preincubation of L-02 cells with Cy-3-G or Pn-3-G significantly alleviated CCl₄-induced injury dose-dependently, exhibited higher cell viability, decreased aminotransferase activity and enhanced cellular antioxidant status. Furthermore, Cy-3-G showed much stronger hepatoprotective activity than Pn-3-G at the same concentration. HPLC analysis showed that Cy-3-G accounted for more than 88% of total anthocyanins in ARBE. These results indicate that ARBE is significantly beneficial to liver health, and that Cy-3-G is the predominant anthocyanin in ARBE exerting this effect. The antioxidant activity of anthocyanins is an important mechanism by which ARBE exerts hepatic health benefit.     

Protective effect of Pracparatum mungo extract on carbon tetrachloride-induced hepatotoxicity in rats

Pracparatum mungo is a traditional and functional food in Traditional Chinese Medicine, especially for treating a variety of liver disorders. In this study, we first report the in vivo hepatoprotective effect of P. mungo extract (PME) on carbon tetrachloride (CCl₄)-induced acute hepatotoxicity in rats. Pre-treatment with PME for 56 days significantly reduced the impact of CCl₄ toxicity on the serum markers of liver damage, aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The results were confirmed histopathologically. In addition, an increased lipid hydroperoxide (LPO), a decreased glutathione (GSH) concentration and a decreased superoxide dismutase (SOD) were observed in the hepatic tissues. On the contrary, treatment of PME prior to the administration of CCl₄ resulted in markedly decreased lipid peroxidation, increased the levels of GSH and SOD in rats. The results indicated that PME has a protective effect against acute hepatotoxicity induced by the administration of CCl₄ in rats, and that the hepatoprotective effects of PME may be due to both the inhibition of lipid peroxidation and the increase of antioxidant activity.     

The in vivo antioxidant and antifibrotic properties of green tea (Camellia sinensis,Theaceae)

The in vivo antioxidant and antifibrotic properties of green tea (Camellia sinensis, Theaceae) were investigated with a study of carbon tetrachloride (CCl₄)-induced oxidative stress and hepatic fibrosis in male ICR mice. Oral administration of green tea extract at doses of 125, 625 and 1250 mg/kg for 8 weeks significantly reduced (p < 0.05) the levels of thiobarbituric acid-reactive substances (TBARS) and protein carbonyls in the liver by at least 28% compared with that was induced by CCl₄ (1 mL/kg) in mice. Moreover, green tea extract administration significantly increased (p < 0.05) the activities of catalase, glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) in the liver. Our study found that oral administration of green tea extract prevented CCl₄-induced hepatic fibrosis, as evidenced by a decreased hydroxyproline level in the liver and a reduced incidence of hepatic fibrosis by histological observations. These results indicate that green tea exhibits potent protective effects against CCl₄-induced oxidative stress and hepatic fibrosis in mice by inhibiting oxidative damage and increasing antioxidant enzyme activities.     

Hepatoprotective effect of the root extract of Decalepis hamiltonii against carbon tetrachloride-induced oxidative stress in rats

Decalepis hamiltonii, a climbing shrub, grows in the forests of peninsular India and is consumed for its health promoting properties. The hepatoprotective activity of the aqueous extract of the roots of D. hamiltonii with known antioxidant constituents was studied against carbon tetrachloride (CCl₄)-induced oxidative stress and liver injury in rats. Pretreatment of rats with aqueous extract of the roots of D. hamiltonii, single (50, 100 and 200 mg/kg b.w.) and multiple doses (50 and 100 mg/kg b.w. for 7 days) significantly prevented the CCl₄ (1 ml/kg b.w.) induced hepatic damage as indicated by the serum marker enzymes (AST, ALT, ALP, and LDH). Parallel to these changes, the root extract also prevented CCl₄-induced oxidative stress in the rat liver by inhibiting lipid peroxidation and protein carbonylation, and restoring the levels of antioxidant enzymes (SOD, CAT, GPx, GR, and GST) and glutathione. The biochemical changes were consistent with histopathological observations suggesting marked hepatoprotective effect of the root extract in a dose dependent manner. Protective effect of the aqueous extract of the roots of D. hamiltonii against CCl₄-induced acute hepatotoxicity could be attributed to the antioxidant constituents.     

Protective effects of dehydroglyasperin c against carbon tetrachloride-induced liver damage in mice

Dehydroglyasperin C (DGC) isolated from licorice has been shown to exhibit antioxidant activity as well as induce phase 2 detoxifying enzymes in mouse hepatoma cells. This study investigated whether or not DGC exerts hepatoprotective effects through modulation of phase 1 and 2 detoxifying enzymes. ICR mice were divided into five groups with 10 mice per group: (1) negative control, (2) positive control injected with carbon tetrachloride (CCl₄, 0.6 mL/kg BW) alone, (3) ICR mice injected with DGC (5 mg/kg BW) alone, (4) ICR mice injected with DGC followed by CCl₄, and (5) ICR mice injected with DGC and CCl₄ simultaneously. Mice were adapted for 1 week, followed by injection with DGC on day 7, CCl₄ on day 8, and sacrifice on day 9 of the experiment. Treatment with DGC induced NQO1 activity in kidney only, but not in the other tissues of mice. Compared to mice injected with CCl₄ alone, mice simultaneously injected with both DGC and CCl₄ showed reduced lipid droplet formation in liver tissue, as assessed by histological examination. Further, DGC demonstrated a slight protective effect against centrilobular injury caused by CCl₄ injection, perhaps through suppression of CYP2E1 expression. In conclusion, DGC possesses hepatoprotective effects against CCl₄-induced injury.     

Collagen peptides from Acaudina molpadioides prevent CCl4-induced liver injury via Keap1/Nrf2-ARE,PI3K/AKT,and MAPKs pathways

Collagen peptide from Acaudina molpadioides (AMP) showed antioxidative activity in H₂O₂-induced RAW264.7 cells in our pervious study. In this study, it was observed that AMP could effectively improve the morphology and function of liver in CCl₄-induced mice. After 200 mg/kg AMP treatment, the content of MDA in liver decreased by 62.3%, and the level of antioxidant enzymes (SOD, GSH-Px, and CAT) increased by more than 65%. Western blot results disclosed that AMP (200 mg/kg) upregulated the Nrf2 level by 73.8% and downregulated Keap1 by 41.0% in CCl₄-induced mice liver. The levels of p-ERK, p-JNK, and p-p38 in 200 mg/kg AMP treatment groups decreased by 57.3%, 40.9%, and 40.6%, but the levels of p-PI3K and p-AKT increased by 162.6% and 60.3%, respectively. Furthermore, the trends of Nrf2, Keap1, p-ERK, p-JNK, p-p38, p-PI3K, and p-AKT levels in H₂O₂-induced RAW264.7 cells after AMP treatment were similar to the results in CCl₄-induced mice liver. These findings provided evidence that AMP exerted antioxidant activity via Keap1/Nrf2-ARE, PI3K/AKT, and MAPKs pathways in vivo and in vitro. Therefore, the collagen peptide from A. molpadioides might represent a novel functional food to prevent acute liver injury via attenuation of oxidative stress.     

Antialcoholic liver activity of whey fermented by Lactobacillus casei isolated from koumiss

Whey fermented liquid (WFL) was studied for its hepatoprotective effects by using chronic alcohol-induced mice. Whey fermented liquid, prepared by inoculating whey with 4% (vol/vol) Lactobacillus casei and then incubating at 41°C for 8 h, was used to orally treat alcohol-induced mice at 3 dosages for 5 wk. Ethanol consumption significantly reduced the activity of superoxide dismutase and glutathione peroxidase, while lowering glutathione content and increasing levels of aspartate aminotransferase, alanine aminotransferase, total triglyceride, malondialdehyde, and cytochrome P450 2E1. Treatment with WFL significantly attenuated the increased levels of alanine aminotransferase, aspartate aminotransferase, triglyceride, and cytochrome P450 2E1, while decreasing superoxide dismutase, glutathione peroxidase, malondialdehyde, and glutathione levels. Pathological changes in the livers of mice who had ingested alcohol were improved by the administration of WFL. These results suggest that WFL may exert a protective effect against alcoholic liver disease by increasing antioxidant activity, which supports the use of WFL as an antialcoholic liver disease treatment.     

美味牛肝菌多糖对急性肝损伤小鼠的保肝作用

用不同剂量的美味牛肝菌多糖(Boletus edulis polysaccharides,BEP)给予小鼠灌胃连续30d后,按10mL/kg剂量腹腔注射含体积分数0.2%CCl4的花生油溶液,建立CCl4诱导小鼠肝损伤模型。测定肝脏指数、肝脏重量、血清谷丙转氨酶(ALT)、谷草转氨酶(AST),以及肝组织中超氧化物岐化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)及还原型谷胱甘肽(GSH)水平,并进一步观察肝脏组织病理学变化。结果表明:BEP能显著抑制CCl4急性肝损伤小鼠肝脏指数、血清ALT、AST水平以及肝脏MDA含量的升高,提高肝脏GSH-Px、SOD及GSH活性,其中800 mg/(kg BW獉d)剂量水平效果最佳,BEP对CCl4急性肝损伤小鼠有一定的保护作用。     

Beneficial effects of yam on carbon tetrachloride‐induced hepatic fibrosis in rats

BACKGROUND: In a previous study, lyophilised yam reduced brain amyloid β‐protein (Aβ) accumulation and improved the antioxidative defence system in senescence‐accelerated (SAMP8) mice. Therefore, the aim of this study was to investigate the hepatic protection of yam in the carbon tetrachloride‐induced hepatic fibrosis of rats. Hepatic fibrosis was induced in rats via intraperitoneal injections of CCl₄ at a dose of 1 mL kg^?1 body weight (BW) twice weekly for 8 weeks. Three groups of rats were gavaged daily with yams at doses of 0.5, 1 and 2 g kg^?1 BW for 8 weeks, respectively. RESULTS: Yam treatments significantly decreased the ratio of liver/body weight, levels of γ‐glutaminotranspeptidase (GGT), low‐density lipoprotein, and triglyceride in serum when compared with those administered CCl₄ alone. Treatment with yams significantly elevated antioxidant activities of glutathione peroxidase (GSH‐Px) and superoxidase dismutase (SOD) in livers. Microscopically, yam‐treated groups presented with low histoscores of CCl₄‐induced liver injury and fibrosis. Additionally, yam treatment reduced the area of GGT‐positive foci and the index of proliferating cell nuclear antigen (PCNA) in liver. CONCLUSION: Daily administration of yam attenuates CCl₄‐induced hepatic fibrosis in rats in a dose‐dependent manner; this attenuation may be related to the antioxidant properties of yams. Copyright © 2009 Society of Chemical Industry     

The in vitro and in vivo antioxidant properties of seabuckthorn (Hippophae rhamnoides L.) seed oil

The antioxidant capacity of seabuckthorn (Hippophae rhamnoides L.) seed oil was investigated with a number of established in vitro assays and in an in vivo study of carbon tetrachloride (CCl₄)-induced oxidative stress in mice. The results showed that DPPH radical scavenging activity, ferrous ion chelating activity, reducing power and inhibition of lipid peroxidation activity all increased with increasing concentrations of seabuckthorn seed oil. Moreover, the EC₅₀ values of seabuckthorn seed oil from the hydrogen peroxide, superoxide radical, hydroxyl radical scavenging assays were 2.63, 2.16 and 0.77 mg/ml, respectively. In the in vivo study, seabuckthorn seed oil inhibited the toxicity of CCl₄, as seen from the significantly increased activities of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. The GSH content in the liver was also increased, whereas hepatic malondialdehyde was reduced. Taken together, these results clearly indicate that seabuckthorn seed oil has significant potential as a natural antioxidant agent.     

Extracts of oyster mushroom (Pleurotus ostreatus) grown on wheat ameliorate hepatotoxicity induced by carbon tetrachloride in rats

Pleurotus ostreatus (PO), which is also called the oyster mushroom, is the secondly most popular cultivated mushroom in the world and has been shown to display antioxidant activity. In this study, the hepatic protective effects of extracts of PO cultured in wheat (POW) on carbon tetrachloride (CCl₄)-induced liver injury in rats were evaluated by analyzing blood markers of liver injury. Sprague-Dawley rats were pretreated with POW extracts (0, 0.5, and 1.0 g/kg) orally for 14 days prior to the administration of CCl₄ for 3 days. Marked evaluation of alanine and aspartate aminotransferases, lactate dehydrogenase, alkaline phosphatase, and γ-glutamyltransferase were observed in the plasma from control rats after CCl₄ treatment. This increased liver injury markers were significantly reduced in a dose-dependent manner by pretreatment with the POW extract, suggesting that POW prevented acute liver damage in CCl₄-intoxicated rats by suppressing cellular leakage and loss of the functional integrity of cell membranes in the liver. POW extracts could also improve lipid profiles damaged caused by CCl₄ in liver through a reducing plasma triglyceride and total cholesterol and a recovering plasma HDL-cholesterol. These results suggest that the extracts of POW ameliorate hepatotoxicity induced by CCl₄ in the rat model.     

Yerba-mate (Ilex paraguariensis) extract prevents ethanol-induced liver injury in rats

Ethanol metabolism-associated oxidative stress contributes to the pathogenesis of alcoholic liver disease. We examined the effect of a Mate tea extract on ethanol-induced liver injury in vitro and in vivo models. Isolated hepatocytes were incubated with ethanol. An extract of Yerba-Mate tea (EMT) was added to the cultures simultaneously with ethanol. EMT treatment suppressed the ethanol-induced increase in cell death by inhibiting cytochrome p450 2E1 (CYP2E1) activity, which is related to the production of reactive oxygen species. Furthermore, we examined the effects of EMT on serum transaminase activity, and the progression of liver fibrosis in rats treated with ethanol and CCl₄. Rats were fed a diet that included 0.005% or 0.02% EMT or no EMT. For a period of 3 weeks, the animals were provided drinking water containing 5% ethanol and were also treated with carbon tetrachloride (CCl₄) (0.1 ml/kg of body weight). EMT treatment suppressed plasma ALT and AST activities in the ethanol- and CCl₄-treated rats. EMT treatment also decreased CYP2E1 expression and increased ADH expression in the ethanol- and CCl₄-treated rats. EMT treatment fully protected the rats against ethanol- and CCl₄-induced liver injury. These results suggest that EMT may serve as a candidate for preventing ethanol-induced liver injury.     

Protective effect of HV-P411, an herbal mixture,on carbon tetrachloride-induced liver fibrosis

This study was performed to examine the anti-fibrotic activity of HV-P411, an herbal mixture of seeds of Vitis vinifera, Schisandra chinensis and Taraxacum officinale extract, against carbon tetrachloride (CCl₄)-induced liver fibrosis. Hepatic fibrosis was induced by intraperitoneal injection of CCl₄ (0.5 ml/kg, twice weekly) for 8 weeks. Rats were treated orally with HV-P411 at 50, 100, 200, and 400 mg/kg once a day. After chronic exposure to CCl₄, the levels of hydroxyproline were markedly increased; these were significantly reduced by HV-P411 at all dose levels. The level of serum aminotransferases and lipid peroxidation were increased after the CCl₄ treatment, while reduced glutathione was decreased. These changes were attenuated by HV-P411. In addition, HV-P411 attenuated CCl₄-induced raised serum concentration of transforming growth factor-β1, and the levels of matrix metalloprotease-2 and tissue inhibitor of metalloprotease-1 mRNAs. Our results suggest that HV-P411 may prevent liver fibrosis by modulating fibrogenesis and fibrolysis.     

Radioprotective effect of radiation-induced Lactococcus lactis cell-free extract against 60Coγ injury in mice

Ionizing radiation (IR) is widely used in the diagnosis and treatment of various cancers. However, IR can cause damage to human health by producing reactive oxygen species. Lactococcus lactis is a type of microorganism that is beneficial to human health and has a strong antioxidant capacity. In this study, the protective effect of normal and IR-induced L. lactis IL1403 cell-free extracts (CFE and IR-CFE, respectively) against oxidative damage in vitro and the radioprotective effect of IR-CFE in vivo was evaluated using ⁶⁰Coγ-induced oxidative damage model in mice. Results showed that IR-CFE exhibited a stronger oxidative damage–protective effect than CFE for L. lactis IL1403 under H₂O₂ in vitro. Moreover, IR-CFE also showed strong radioprotective effect on hepatocyte cells (AML-12) under radiation condition, and the effect was better than that of CFE. Animal experiment indicated that IR-CFE could reduce the IR-induced damage to the hematopoietic system by increasing the number of white blood cells and red blood cells in peripheral blood of irradiated mice. It was also observed that IR-CFE could markedly alleviate the ⁶⁰Coγ-induced oxidative stress via increasing the activities of superoxide dismutase and glutathione peroxidase, enhancing the levels of glutathione, and decreasing the contents of malondialdehyde in serum, liver, and spleen. In addition, IR-CFE also could reduce the activities of alanine transaminase and aspartate aminotransferase in serum, thereby reducing radiation damage to the liver. These results suggested that IR-CFE could be considered as potential candidates for natural radioprotective agents. This study provides a theoretical basis for improving the application of lactic acid bacteria.     

Disodium Guanylate Alleviates Acute Hepatic Injury Induced by Carbon Tetrachloride Via Antioxidative Stress and Antiapoptosis In Vivo and In Vitro

Hepatic injury is one of the most common digestive system diseases worldwide in clinic. Guanylic acid or guanosine monophosphate (GMP) was an important component of nucleotides, which is mainly in the form of sodium salt (disodium guanylate, GMP‐Na₂). However, its effect on hepatic injury has not yet been investigated. This study is to investigate the protective effects of GMP‐Na₂ on acute hepatic injury induced by carbon tetrachloride (CCl₄), and to explore its mechanism. The hepatic injury models of mice and HL‐7702 cells were induced by CCl₄. The alanine transaminase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), malondialdehyde (MDA), total antioxidant capacity (T‐AOC) were determined by biochemical method. Hematoxylin–eosin staining were used to determine the morphological changes on liver tissue in mice. The mRNA and protein expressions of caspase‐3, Bax, and Bcl‐2 were detected by RT‐PCR and Western blot analysis. Our results show that GMP‐Na₂ treatment significantly decreased the activities of ALT and AST, and the levels of MDA as well as increased the levels of SOD, GSH‐Px, and T‐AOC. Importantly, GMP‐Na₂ effectively enhanced the antiapoptosis function by upregulating Bcl‐2 expression and downregulating caspase‐3 and Bax expressions in vivo and in vitro. Moreover, the histopathological changes of liver tissue were obviously improved after GMP‐Na₂ treatment. These findings suggest that GMP‐Na₂ has protective effects on hepatic injury, and its mechanisms may be associated with antioxidative stress and antiapoptosis.     

Prevention of ethanol-induced hepatotoxicity by fermented Curcuma longa L. in C57BL/6 mice

The protective effect of fermented Curcuma longa L. (FC) was investigated in male C57BL/6 mice under ethanol-induced oxidative stress. Ethanol markedly elevated levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in mice. However, mice receiving FC prior to ethanol treatment did not display hepatotoxicity as evidenced by the significant reductions of AST and ALT activities. When compared to the ethanol-alone treated group, FC group exhibited a significant decrease in cytochrome P-450 2E1 (CYP2E1) activity, an enzyme associated with oxidative stress. Indicators of the hepatic antioxidant defense system, such as levels of superoxide dismutase, catalase, glutathione reductase and glutathione were also increased in FC-pretreated mice. The amelioration of malondialdehyde was indicative of the protective effect of FC against liver damage mediated by ethanol. These results suggest that FC could be a candidate used for the prevention against alcoholic liver diseases by the alleviation of oxidative stress via suppressing CYP2E1.