• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.1
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• pp.87-91
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• 2002

This study was designed to investigate the effects of Hijikia fusiforme (Harvey) Okamura ethanol extract on the ethanol-induced hepatotoxicity of rat administered orally experimental diets for 6 weeks. Sprague-Dawley rats weighing about 100 g were divided into 4 groups; normal group (NOR), ethanol (35% ethanol 10 mL/kg b.w/day) treated group (CON), ethanol and Hijikia fusiforme ethanol extract 200 mg/kg (HE1) and 400 mg/kg (HE2) concomitantly treated group, respectively. Each group was examined for the growth rate, feed efficiency ratio (FER), activities of antioxidative enzymes and contents of TBARS and glutathione. Hijikia fusiforme ethanol extract showed increasing effects of the growth rate by 43%, and FER was gradually increased by Hijikia fusiforme ethanol extract treatment, compard with ethanol treatment. Ethanol elevated the activities of superoxide dismutase, catalase and glutathione peroxidase of rat liver markedly as compared to normal group, but those activities were significantly decreased in Hijikia fusiforme ethanol extract treatment by 56%, 38% and 25%, respectively. Xanthine oxidase activity elevated by ethanol was not affected by Hijikia fusiforme ethanol extract. The content of TBARS increased by ethanol treatment was signigicantly decreased in HE2, and the glutathione content depleted by ethanol treatment was increased by Hijikia fusiforme ethanol extract administration adjacent to normal level. These results suggest that Hijikia fusiforme ethanol extract is believed to be a possible protective effect for the ethanol-induced hepatotoxicity of rat liver.

• Toxicological Research
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• v.16 no.1
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• pp.63-66
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• 2000

The effects of acute ethanol on the high K+ induced $Ca^{2+}}$ signals were examined from primary cultures of cerebellar granule neurons. $Ca^{2+}}$ signals were measured with Calcium Green-1 based microscopic video imaging. Because $Ca^{2+}}$ signal was low in most of granule neurons without stimuli, high KCI was used for depolarization. In most case, acute exposure to ethanol reduced the peak amplitude of the $Ca^{2+}}$ signals, induced by high K+, even though low concentration of ethanol(2~10mM) was used and the effects lasted more than 30min. In was also possible to see differences of ethanol inhibition, i.e. the temporal pattern of $Ca^{2+}}$ signal reductions and the strength of inhibition of $Ca^{2+}}$ signals in cerebellar granule neurons. These results indicate that low concentration of ethanol has diverse actions on the $Ca^{2+}}$ signals in cerebellar granule neurons.

• Journal of Food Hygiene and Safety
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• v.7 no.2
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• pp.83-89
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• 1992

This study was perfonned to investigate effectiveness eness on the gastritis and gastric lesion with the methanol extract of the flower buds of Eugenio caryophyllata. The extract was fractionated with hexane, chIorofonn, ethyl acetate, butanol, followed by bioassay Oil antigastritis. The ethyl acetate and the buthanol fraction reduced significantly HCI.ethanol induced gastric lesion at the dose of 165 and 215 mg/kg, p.o., respectively. These results may indicate that remarkably.effective are ethyl acetate and butanol fractions in HCI-ethanol induced gastric lesion. Howeever, the fractions didn't exhibit any inhibition of gastric secretion and acid output. The buthanol fraction reduced significantly the acetic acid induced ulcer at a daily dose of 215 mg/Kg, p.o., given for 10 days. These result showed considerable inhibit of acetic acid induced ulcer without inhibition of indomethacin induced gastric lesion. The methanol extract showed low acute toxicity with minimum lethal dose of more than 3000 mg/kg, p.o. in mice. In conclusion, Eugenia F10s exhibited antigastric activity which might be attributable to inhibition of gastric secretion. It is indicated that activie component may be present in the buthanol fraction.

• Journal of the Korean Applied Science and Technology
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• v.30 no.3
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• pp.394-399
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• 2013

This study was performed to investigate the antidiabetic study effect in ethanol extract of Ailanthicortex(A.C) radici in Streptozotocin(STZ)-induced diabetic rats. Diabetes was induced by intravenous injection of STZ at a dose of 45mg/kg dissolved in citrate buffer. The ethanol extract of A.C radici was orally administrated once a day for 7 days at a dose of 500mg/kg. The content of serum glucose, triglyceride(T.G), total cholesterol were significantly decreased in treated group compared to the those of STZ-control group. The content of hepatic glycogen and activity of glucokinase(GK) were significantly increased in treated group compared to the those of STZ-control group. but activity of glucose-6-phosphate dehydrogenase(G-6-PDH) was significantly increased. These results indicated that ethanol extract of A.C would have antidiabetic effect in STZ-induced diabetic rats.

• Journal of Food Hygiene and Safety
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• v.31 no.1
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• pp.1-7
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• 2016

In the present study, our aim was to determine whether green tea extract (GTE) and its major constituent, epigallocatechin-3-gallate (EGCG) have a protective effect on ethanol-induced cytotoxicity and DNA damage in NIH/3T3 and HepG2 cells. The cell viability and DNA single strand breaks were examined by MTT assay and alkaline single cell gel electrophoresis (Comet assay), respectively. Ethanol decreased the cell viability and also increased DNA single strand breaks in a concentration-dependent manner. On the other hand, GTE showed the protective effect of cytotoxicity and DNA damage induced by ethanol in both cell lines. GTE and EGCG, were found to possess the anti-oxidative and anti-genotoxic activities by evaluation with DPPH test, LDL oxidation assay, oxidative DNA damage assay and 8OH-2'dG generation test. These results were also verified by the experimental results demonstrating the lower cytotoxicity and genotoxicity of commercial green tea liqueur compared to pure ethanol in same concentration. Thus it is concluded that the supplementation of GTE or EGCG may mitigate the ethanol-induced cytotoxicity and DNA damage.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.4
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• pp.907-911
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• 1999

To evaluate the effect of defatted sesame flour(DSF) on the oxidative stress of ethanol feeding in rats, Wistar male rats were divided into 4 groups of control, ethanol, DSF and DSF ethanol. Each group was sacrificed after feeding for 4 weeks and was examined by measuring the formation of 2 thiobarbituric acid reactive substance(TBARS), total cholesterol(TC) in serum, redox glutathione S transferase(GST) enzyme activity and the contents of glutathione(GSH) in the liver. The formation of TBARS in the liver after ethanol feeding was significantly increased comparing to the control, but the levels were significantly decreased by the DSF as compared to the ethanol feeding group(p<0.05). When compared to fed control diet, we found that serum TC levels were significantly lower in the DSF fed group than control group (p<0.05). The activity of hepatic GST was significantly increased by DSF as compared to the control and was decreased by ethanol feeding. On the other hand, the hepatic contents of GSH were unaffected by DSF feeding. Our findings suggest that feeding DSF may inhibit ethanol induced oxidative stress may be due to the stimulation of antioxidative activity by sesaminol glucosides in DSF.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.6
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• pp.805-811
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• 2016

This study was conducted to investigate the protective effects of water extract from Crassostrea gigas (CGW) against ethanol-induced hepatic toxicity in rats. Seventy-two male Wistar rats (6-week-old) were divided into six groups of 12 animals each: control group (1 mL saline/d), ethanol-treated group, positive control group (ethanol+Hovenia dulcis Thunb extract), CGWL group (ethanol+low dosage of CGW), CGWM group (ethanol+medium dosage of CGW), and CGWH group (ethanol+high dosage of CGW). All groups except the control group received ethanol (40% ethanol 5 g/kg) orally. CGW administration with ethanol resulted in prevention of ethanol-induced hepatotoxicity by increasing levels of serum alanine aminotransferase and ${\gamma}-glutamyltransferase$. CGW supplementation significantly reduced formation of malonaldehyde and inhibited reduction of hepatic glutathione and peroxidase levels, as compared with the ethanol-administration group. Further, CGW suppressed expression of CYP2E1, which was elevated by ethanol administration. Consequently, our results indicate that Crassostrea gigas may exert hepatoprotective effects against alcohol-induced hepatocyte injury by intensifying the anti-oxidative defense system.

• Journal of Microbiology and Biotechnology
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• v.33 no.4
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• pp.463-470
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• 2023

This study confirmed the change in functional composition and alcohol-induced acute liver injury in Aloe arborescens after fermentation. An acute liver injury was induced by administration of ethanol (3 g/kg/day) to C57BL/6J mice for 5 days. A fermented A. arborescens Miller leaf (FAAL) extract was orally administered 30 minutes before ethanol treatment. After fermentation, the emodin content was approximately 13 times higher than that of the raw material. FAAL extract significantly attenuated ethanol-induced aspartate aminotransferase, alanine aminotransferase, and triglyceride increases in serum and liver tissue. Histological analysis revealed that FAAL extract inhibits inflammatory cell infiltration and fat accumulation in liver tissues. The cytochrome P450 2E1, superoxide dismutase, and glutathione (GSH), which involved in alcohol-induced oxidative stress, were effectively regulated by FAAL extract in serum and liver tissues, except for GSH. FAAL also maintained the antioxidant defense system by upregulating heme oxygenase 1 and nuclear factor erythroid 2-related factor 2 protein expression. In addition, FAAL extract inhibited the decrease in alcohol dehydrogenase and aldehyde dehydrogenase activity, which promoted alcohol metabolism and prevented the activation of inflammatory response. Our results suggest that FAAL could be used as a potential therapeutic agent for ethanol-induced acute liver injury.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.2
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• pp.154-159
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• 2009

The hepatoprotective effect of ethanol extract from Hovenia dulcis fruit (HD) against ethanol-induced oxidative damage was investigated. Ethanol-induced reactive oxygen species (ROS) generation and liver damage on HepG2/2E1 cells were protected by $100{\mu}g/mL$ ethanolic extract from HD. Male C57BL/6 mice were divided into 3 groups; control (NC), ethanol (ET), ethanol plus 1 g/kg body weight ethanolic extract of HD (ET-HD). The activities of serum alanine amintransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were significantly increased in ethanol-treated group. However, ET-HD group showed protective effect by lowering serum activities. The ET group markedly decreased the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione-s-transferase (GST) with the reduced level of glutathione (GSH) in liver. On the other hand, ET-HD group increased the activities of SOD and GST, and the level of GSH. Lipid peroxidation level, which was increased after ethanol administration, was significantly reduced in ET-HD group. Based upon these results, it could be assumed that ethanolic extract of HD protected the liver against ethanol-induced oxidative damage by possibly inhibiting the suppression of antioxidant activity and reducing the rate of lipid peroxidation in vitro and in vivo. Therefore, extract of Hovenia dulcis fruit might be used as a protective agent for ethanol-induced hepatic damages.

• Korean Journal of Veterinary Service
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• v.26 no.4
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• pp.345-359
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• 2003

A number of toxicants have been incriminated as a causing hepatic disease. Among many detrimental injury, alcohol has been noted for hepatitis, fatty liver, fibrosis, and hepatic cirrhosis. The purpose of this study was to develop animal model for hepatic fibrosis in pigs fed ethanol, and to search for a new anti-fibrogenic agent via this model. Twelve male Landrace pigs were divided into 3 groups of 4 animals each. Group 1, 2 and 3 were fed with active ceramic water only, ceramic water + liquid diet containing 15% ethanol and normal tap water + liquid diet containing 15% ethanol for 12 weeks, respectively. At week 12, all pigs were immediately sacrificed for collection each tissue and blood. Serologically, serum ALT and AST levels were significantly reversed in group 2, as compared to group 3. They were normal range in pigs of group 1. Microscopically, macrovesicular lipid droplets and moderate hepatocellular necrosis were evident in the tap water + ethanol fed group 3. However, the active ceramic water treated group 1 showed normal architecture. Moreover, in group 2, mild fatty changes and necrosis were observed in hepatocytes. Collagen fibers were increased in spaces surrounding periportal and interlobular connective tissues in the group 3 of tap water + ethanol, but collagen synthesis and its thickness of fibrotic septa connecting portal tracts were markedly reduced in the group 2 of ceramic water + ethanol. Myofibroblasts were detected mainly in the interlobular connective tissues of pig liver of group 3 treated ethanol and tap water. Few to no myofibroblasts were observed in groups 1 and 2. CYP2E1 was not or rarely detected in group 1 fed ceramic water. However, group 2 showed slightly activation of CYP2E1 in the area of pericentral vein, while CYP2E1 was significantly activated in group 3 fed tap water and ethanol. Based on the above data, we believe that we have developed a unique alcohol induced fibrosis model in pig, which will be useful in developing anti-fibrotic agents and drugs. Furthermore, the active ceramic water used in our study had an inhibitory and may be protective against ethanol induced hepatic toxicity and fibrosis.