• YAKHAK HOEJI
• /
• v.34 no.4
• /
• pp.267-276
• /
• 1990

To achieve a better understanding of antioxidant action manifested by malotilate, the dithiol malonates, we monitored the oxy radical-scavenging system against the chronic hepatic damage induced by $CCl_4$ alone or in combination with ethanol. Malotilate was given orally at a dose of 100 mg/kg/day and $CCl_4$ 1.5 ml/kg was injected subcutaneously twice a week for 4 weeks. In each group receiving ethanol, drinking water was replaced by 20% aqueous solution or glucose, isocaloric amounts of ethanol, as a control of ethanol was diluted in its drinking water. Each rat was killed as a starved state at 18 hours after the period of the experiment, four weeks. The results were summarized as follows: 1) Malotilate inhibited the rate of generation of superoxide radicals, the accumulation of lipoperoxides, and promoted the synthesis of glutathione in the liver. 2) Malotilate stimulated the enhancement of activity of superoxide dismutase in hepatic mitochondria. 3) Malotilate had no effects on the hepatic $H_2O_2$ contents. 4) Malotilate showed the increase of catalase activity in the liver poisoned with $CCl_4$, and also gave a tendency to increase it in the liver intoxicated with ethanol. Thus, our data suggested that the activation of hepatic antioxidant system in the presence of malotilate would play a role in protecting liver against the toxic effects of oxy radical and/or lipid peroxides under the hepatotoxic conditions induced by $CCl_4$ with or without ethanol. However, the effects of malotilate against the ethanol-induced hepatotoxicity appear to be insignificant.

• Food Science and Preservation
• /
• v.21 no.3
• /
• pp.412-420
• /
• 2014

This study was performed to investigate the effect of fermented Hovenia dulcis Thunb fruit water extract on biomarkers for acute (a) ethanol-induced hangover and chronic (c) ethanol-induced liver injury in rats. For acute ethanol-induced hangover, the rats were administered distilled water (D.W., 10 mL/kg body wt.), Hovenia dulcis Thunb fruit water extract (HWE, 400 mg/10 mL/kg body wt.) and fermented HWE (FHWE, 400 mg/10 mL/kg body wt.), respectively, before 40% ethanol (5 g/kg body wt.) was administered. For chronic ethanol-induced liver injury, the rats were randomly divided into the normal control (cNC), ethanol (cET), cET-HWE and cET-FHWE groups. The cNC and cET groups were administered D.W. (10 mL/kg body wt.) before 40% alcohol (5 g/kg body wt.) was administrered for 21 days. The cET-HWE and cET-FHWE groups were administered HWE (400 mg/10 mL/kg body wt.) and FHWE (400 mg/10 mL/kg body wt.), respectively before 40% ethanol (5 g/kg body wt.) administration for 21 days. For acute ethanol-induced hangover, the serum alcohol and acetaldehyde concentrations were more significantly reduced in the aHWE and aFHWE groups than in the aET group. Moreover, the effect of FHWE was greater than that of HWE. For chronic ethanol-induced liver injury, the serum ethanol, acetaldehyde, ${\gamma}$-glutamyl transpeptidase (${\gamma}$-GTP) levels and the hepatic lipids concentration more significantly dropped in the cET-HWE and cET-FHWE groups than in the cET group. The FHWE administration showed faster recovery of the serum glucose concentration than in the cET and cET-HWE groups. The body weight reduction tended to normalize in the cET-HWE and cET-FHWE groups, which is ideal for chronic ethanol administration. These results suggest that FHWE has a protective effect against ethanol-induced liver damage, as evidenced by its ability to lower the serum ethanol and acetaldehyde concentrations after alcohol administration, and by its ability to decrease the level of ${\gamma}$-GTP and hepatic lipids. FHWE also elevated serum glucose concentration. Therefore, FHWE is effective in reducing ethanol-induced hangover and can play a beneficial role in the treatment of ethanol-induced liver damage as well as body weight reduction.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.27 no.5
• /
• pp.611-616
• /
• 2013

Alcoholic liver disease (ALD) is a major cause of morbidity and mortality around the world. Although much progress has been made in understanding the pathogenesis of ALD, there remains no effective therapy for it. Accumulated evidence indicates that oxidative stress is the main pathological factors in the development of ALD. Ethanol administration causes accumulation of reactive oxygen species (ROS), including superoxide, hydroxyl radical, and hydrogen peroxide. ROS, in turn, cause lipid peroxidation of cellular membranes, and protein and DNA oxidation, which results in hepatocyte injury. In addition to pro-oxidants formation, antioxidants depletion caused by ethanol administration also results in oxidative stress. The objective of this study is to investigate the effects of Shiryung-tang extract on the chronic alcoholic liver injury induced by EtOH. Male Sprague Dawley rats were used in this study. All rats were maintained under standard laboratory conditions ($23{\pm}1^{\circ}C$, 12h light/12h dark cycles). All animals (n=30) were randomly divided into following groups: (1) Normal group, treated with distilled water (n=10); (2) Control group, treated with ethanol (n=10); (3) Sample group, treated with ethanol + pharmacopuncture (n=10). For oral administration of ethanol in Control and Sample group, the ethanol was dissolved in distilled water in concentrations of 25%(v/v). Throughout the experiment of 8 week, the rats were allowed free access to water and standard chow. Sample group were administrated by Shiryung-tang extract daily for 8 weeks. Control group were given normal saline for same weeks. As a results, the oral administration of ethanol for 8 weeks leads to hepatotoxicity. The levels of hepatic marker such as HDL-cholesterol, triglyceride, aspartate aminotransferase and alanine aminotransferase were altered. The ethanol also increased lipid peroxidation and depletion of antioxidant enzyme activities as well as hepatic tissue injury. However, the treatment of Shiryung-tang extract prevented all the alterations induced by ethanol and returned their levels to near normal. These data suggest that Shiryung-tang extract could have a beneficial effect in inhibiting the oxidative damage induced by chronic ethanol administration. Therefore, Shiryung-tang extract can be a candidate to protect against EtOH-induced liver injury.

• Preventive Nutrition and Food Science
• /
• v.9 no.4
• /
• pp.352-360
• /
• 2004

To investigate the antioxidative effects of an etbylacetate fraction extracted from the flowers of Chrysanthemum indicum L. (Chrysanthemi Flos) on the antioxidative system and lipid profiles of rats with ethanol induced hepatotoxicity. Sprague-Dawley rats weighing $100\~150$ g were divided into 5 groups: normal group (NOR), Chrysanthemi Flos EtOAC fraction (200 mg/kg) treated group (S1), $35\%$ etbanol (10 mL/kg) treated group (S2), Chrysanthemi Flos EtOAC fraction (200 mg/kg) and ethanol concomitantly treated group (S3) and Chrysanthemi Flos EtOAC fraction (400 mg/kg) and ethanol concomitantly treated group (S4), respectively. The antioxidative activity of each fraction was decreased in order of EtOAC, n-hexane, n-BuOH, water and chloroform. The growth rates and feed efficiency ratios were decreased by ethanol treatment, but were gradually restored to similar levels as in the NOR group by administering Chrysanthemi Flos EtOAC fraction. The whole blood concentrations of total cholesterol and LDL-cholesterol, and the activities of ALT and AST that were elevated by ethanol were significantly decreased in the Chrysanthemi Flos EtOAC fraction treated groups. It was also observed that the activities of SOD, catalase, xanthine oxidase and GSH-Px elevated by ethanol in rat liver were markedly decreased in the Chrysanthemi Flos EtOAC fraction treated group as compared to S2. These results suggest that Chrysanthemi Flos EtOAC fraction has possible protective effects against ethanol induced hepatotoxicity in rat liver.

• Journal of Haehwa Medicine
• /
• v.9 no.1
• /
• pp.135-142
• /
• 2000

For the evaluation of protective effect on hepatic damage by Korean red ginseng mixed formula, we used GR(Korean red ginseng), GRF-A(Korean red ginseng-mixed formula) as a materials. The study was performed on protective effect against hepatic damage induced by $CCl_4$. In vitro assay with 1.1 mM galactosamine, protection(%) was 44%(GR), 58%(GRF-A) at 50ug/ml, while maxium protection(%) was 5%(GR) and 24% (GRF-A) against acute hepatotoxicity by $CCl_4$. GRF-A significantly protected ethanol induced-liver damage by lowering ALT and ALP and fatty degenertion in liver tissue.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.38 no.10
• /
• pp.1347-1352
• /
• 2009

The effects of methanol extract of barely (Hordeum vulgare) on alcohol-induced damages of liver were investigated in male ICR mice. Mice were divided into three groups, control, ethanol, and ethanol plus 0.15% of barley extract. After four weeks of ethanol feeding, ethanol group significantly increased the P450 content, CYP2E1 and CYP1A2 enzyme activities, whereas ethanol plus barely group markedly decreased to levels similar to control group. Catalase activity in ethanol group was significantly lower than that in control group; however, ethanol plus barely group stimulated catalase activity as well as SOD activity significantly. These results indicated that barely extract modulated P450 enzymes for ethanol-induced liver damage and might be useful in developing functional food for alcoholic liver damage.

• Journal of Acupuncture Research
• /
• v.32 no.1
• /
• pp.13-22
• /
• 2015

Objectives : Alcohol-related liver disease is a major cause of morbidity and mortality worldwide. The present study was undertaken to determine whether Ganoderma lucidum pharmacopuncture(GLP) could protect against chronic liver injury induced by ethanol intoxication in rats. Methods : Sprague-Dawley rats were divided into 4 groups: normal, control, normal saline pharmacopuncture(NP), and GLP, with 8 animals in each. Each group, except normal, received ethanol orally. The NP and GLP groups were treated daily with NP and GLP respectively. The control group was not treated. All rats except the normal group were intoxicated for 4 weeks by oral administration of EtOH(6 g/kg BW). Two acupuncture points were used: Qimen($LR_{14}$) and Taechung($LR_3$). Body weight, histopathological analysis, liver function, activities of antioxidant enzymes, and immunohistochemistry were assessed. Results : GLP reduced the histological changes due to chronic liver injury induced by EtOH and significantly reduced the increase in the alanine aminotransferase(ALT) and aspartate aminotransferase(AST) enzymes. It significantly reversed the superoxide dismutase(SOD) and the catalase activities(CAT). It also significantly decreased BAX and increased Bcl-2 immunoreactivity expression. Conclusions : This study showed the protective efficacy of GLP against EtOH-induced chronic liver injury in SD rats by modulating ethanol metabolizing enzymes activity, attenuating oxidative stress, and inhibiting mitochondrial damage-mediated apoptosis.

• Advances in Traditional Medicine
• /
• v.7 no.3
• /
• pp.297-303
• /
• 2007

The ethyl acetate fraction (EAF) and n-butanol fraction (NBF) of ethanolic extract of Bacopa monnieri aerial parts were screened for hepatoprotective activity and in vivo antioxidant activity on ethanol-induced hepatotoxic rats. Ethyl acetate fraction was found to be more potent even though both the fractions were endowed with significant hepatoprotective activity. EAF and NBF were investigated for hepatoprotective activity in albino rats at 300 mg/kg, p.o. dose and compared with standard drug Silymarin (25 mg/kg, p.o.). Results show that both the fractions were effective in blunting ethanol-induced enhanced activities of serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, alkaline phosphatase, level of serum bilirubin (both total and direct), liver weight loss and was also effective in reducing ethanol-induced lipid peroxidation both in vitro and in vivo. Furthermore, the fractions could also enhance ethanol-induced suppressed activities of superoxide dismutase, catalase and decreased level of reduced glutathione. Results of hepatocellular damage caused by ethanol and its recovery by EAF and NBF, suggest that they might be considered as a potential source of natural hepatoprotective agents, which could be related to the free radical scavenging properties of saponins present in high concentration in the fractions.

• International Journal of Industrial Entomology and Biomaterials
• /
• v.35 no.2
• /
• pp.123-128
• /
• 2017

Hangover due to alcohol consumption causes social and physical problems. There is a growing interest in edible insects worldwide. We have previously published a new technology to make hard mature silkworm, Bombyx mori, into edible form, steamed and freeze-dried mature silkworm larval powder (SMSP). In this study, AIN-76 or SMSP (0.1 and 1 g/kg rat body weight) containing diets in SD rats were pretreated for 2 weeks, and ethanol (3 g/kg rat body weight) was administered as an oral gavage and sacrificed after 3 hours. As a result, blood alcohol and aldehyde levels were significantly decreased in SMSP fed rats. In addition, liver injury markers, alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly decreased in SMSP group compared to ethanol group. $TNF-{\alpha}$, an inflammatory cytokine, and malondialdehyde (MDA), an oxidative stress marker, also showed a dose-dependent decrease in the group receiving SMSP. Conclusively, consumption of SMSP not only reduced hangover induced by ethanol, but also decreased liver damage, oxidative stress, and inflammatory response.

• Journal of Applied Biological Chemistry
• /
• v.63 no.4
• /
• pp.413-420
• /
• 2020

We studied the effects of the extract of aerial parts of hydroponically cultured ginseng (HGE) on alcohol-induced liver damage (AILD) in mice. AILD was induced by the oral administration of ethanol (EtOH) (25%; 5 g/kg body weight) for seven days in the study as well as EtOH-only groups. However, HGE (4 and 12 mg/kg) was orally administered (once daily for ten consecutive days) only to the study group, three days prior to the EtOH treatment. The HGE-treated group showed significantly lower levels of alanine aminotransferase and aspartate aminotransferase than the EtOH-only group. In addition, HGE administration decreased the level of serum lactate dehydrogenase, a known marker of liver damage. The effect of HGE on AILD was found to be dose dependent, and the consecutive administration of HGE showed no side effects in mice. Our study indicates that HGE treatment can potentially reduce oxidative stress and toxicity in the liver of alcohol-treated mice and that HGE can be a useful therapeutic agent for alcohol-induced hepatotoxicity. Additionally, a simple and efficient high-performance liquid chromatography-ultraviolet detection method was developed for determining the contents of four major ginsenosides in HGE. The aerial parts of hydroponically cultured ginseng were extracted using 70% fermented ethanol, and the contents of ginsenosides F5, F3, F1, and F2 in HGE were found to be 2.5, 4.4, 1.4, and 23.3 mg/g, respectively.