• 약학회지
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• 제58권5호
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• pp.300-306
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• 2014

Ethanol consumption causes psychomotor alterations. Hovenia Semen seu Fructus (HS), widely distributed in Korea, China, and Japan, has been reported to have beneficial effects on acute alcohol-induced liver injury. The present study sought to assess the effects of HS extract on ethanol-induced psychomotor alterations in rats. Sprague-Dawley rats were orally (p.o.) given ethanol (4 g/kg) (ethanol group) to induce psychomotor alterations. A separate group (HS-treated groups), were treated with different dosages of HS (50, 100, and 200 mg/kg, p.o.), 30 minutes before ethanol treatment. The control group received only the vehicle (saline). Ethanol-induced psychomotor alterations were evaluated in the open-field, rota-rod, hanging wire, and cold swimming test. In addition, blood ethanol and acetaldehyde concentrations were also measured. Behavioral evaluations and blood analysis were carried out 0.5, 1, 2, 4, and 8 hours after ethanol administration. Pre-treatment of HS ameliorated ethanol-induced alterations in the open-field, rota-rod, and cold swimming test, significantly evident in 2 and 4 hours after ethanol treatment. These improvements coincided with decrease in blood ethanol and acetaldehyde concentration. Based on these results, the present study suggests that HS may have ameliorating effects against ethanol-induced psychomotor alterations.

• 한국식품영양과학회지
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• 제23권5호
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• pp.750-756
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• 1994

The effect of onion juice on ethanol -induced lipid peroxidation were studied were studied in rats. The contents of thiobarbituric acid (TBA) -reactants increased significantly in liver thanol(4ml/kg/day) administered -rats. The activities of serum alanine aminotransferase and alkaline phosphatase increased by ethanol administration compared with control group, but alterations of antioxidant enzymes activities in liver of ethanol administered rats were not significant vs control group. The glutathione contents in liver decreased by ethanol , whereas the glutathione level increased in ethanol and onion juice group compared with ethanol group. The contents of hepatic TBA-reactants and serum aminotrasnferase activity in ethanol group were reduced by onion juice administration. In these results, increased hepatic TBA-reactants of liver in ethanol group might be due to decreased glutathione contents in liver. Reduced glutathione (GSH) plays an important roles in the liver in several detoxification and the reduction of lipid peroxides. So the protective effects of onion juice on ethanol-induced increment of TBA-reactants may be due to the increament of lgutathions content. The glutathione depletion by ethanol was an important factor of ethanol-induced cell damage, and the prevention of onion juice to the glutathione depletion reduced by ethanol may be an important factor on the protection from ethanol-induced lipid perpxidation in rats.

• 약학회지
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• 제45권6호
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• pp.677-682
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• 2001

investigate action of ethanol on histamine release from rat peritoneal mast cells, we compared the inhibitory effect of ethanol with those of calcium antagonists in mechanism of between ATP and compound 48/80-induced histamine release. Ethanol dose-dependently inhibited 100 ${\mu}{\textrm}{m}$ ATP-induced histamine release, whereas did not inhibit 1 $\mu\textrm{g}$/ml compound 48/80-induced histamine release. Verapamil, TMB-8 and EGTA dose-dependently inhibited ATP-induced histamine release, but did not inhibit compound 48/80-induced histamine release. Such an inhibitory effect of calcium antagonist was similar to that of ethanol. These results suggest that the inhibitory effect of ethanol on histamine release from rat peritoneal mast cells is mediated via disturbance of calcium mobilization..

• Biomolecules & Therapeutics
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• 제24권4호
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• pp.433-437
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• 2016

Consumption of high doses of ethanol can lead to amnesia, which often manifests as a blackout. These blackouts experienced by ethanol consumers may be a major cause of the social problems associated with excess ethanol consumption. However, there is currently no established treatment for preventing these ethanol-induced blackouts. In this study, we tested the ethanol extract of the roots of Salvia miltiorrhiza (SM) for its ability to mitigate ethanol-induced behavioral and synaptic deficits. To test behavioral deficits, an object recognition test was conducted in mouse. In this test, ethanol (1 g/kg, i.p.) impaired object recognition memory, but SM (200 mg/kg) prevented this impairment. To evaluate synaptic deficits, NMDA receptor-mediated excitatory postsynaptic potential (EPSP) and long-term potentiation (LTP) in the mouse hippocampal slices were tested, as they are known to be vulnerable to ethanol and are associated with ethanol-induced amnesia. SM (10 and $100{\mu}g/ml$) significantly ameliorated ethanol-induced long-term potentiation and NMDA receptor-mediated EPSP deficits in the hippocampal slices. Therefore, these results suggest that SM prevents ethanol-induced amnesia by protecting the hippocampus from NMDA receptor-mediated synaptic transmission and synaptic plasticity deficits induced by ethanol.

• 동의생리병리학회지
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• 제26권1호
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• pp.67-73
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• 2012

The exposure of gastric mucosa to ethanol produces acute ulcers mediated by inflammatory processes, hemorrhagic erosions and increase of reactive oxygen species. The purpose of this study was to assess the effects of Coptidis Rhizoma(CR) aqueous extracts on hydrochloride (HCl)/ethanol induced gastric ulcer in mice as compared with rebamipide (30 mg/kg) and ranitidine (100 mg/kg). Stomach ulcers were induced by oral ingestion of HCl/ethanol. CR extracts (125, 250 and 500 mg/kg) were orally administered, once a day for 7 continuous days, and 1 hr after last 7th treatment of CR extracts stomach ulcers were induced. Effects of CR extracts on HCl/ethanol-induced gastric ulcer were evaluated based on gross and microscopic observations with anti-oxidant activities. All three different dosages of CR extract significantly decreased HCl/ethanol-induced gastric ulcer compared with the HCl/ethanol control mice. CR extracts also strengthened the antioxidative defense systems - decreased the level of lipid peroxidation but increased the level of catalase, superoxide dismutase and nitrate/nitrite compared with the HCl/ethanol control. The effects of CR extract 500 mg/kg were similar to that of 30 mg/kg rebamipide, and CR extract 250 mg/kg showed similar anti-ulcer effects as compared with ranitidine 100 mg/kg. These results suggest that the gastroprotective effects of CR extracts on mice ulcer models can be attributed to its ameliorating effect on oxidative damages.

• Biomolecules & Therapeutics
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• 제20권5호
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• pp.492-498
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• 2012

Phytochemicals have been known to exhibit potent antioxidant activity. This study examined cytoprotective effects of phytochemicals including quercetin, catechin, caffeic acid, and phytic acid against oxidative damage in SK-Hep-1 cells induced by the oxidative and non-oxidative metabolism of ethanol. Exposure of the cells to excess ethanol resulted in a significant increase in cytotoxicity, reactive oxygen species (ROS) production, lipid hydroperoxide (LPO), and antioxidant enzyme activity. Excess ethanol also caused a reduction in mitochondrial membrane potential (MMP) and the quantity of reduced glutathione (GSH). Co-treatment of cells with ethanol and quercetin, catechin, caffeic acid and phytic acid significantly inhibited oxidative ethanol metabolism-induced cytotoxicity by blocking ROS production. When the cells were treated with ethanol after pretreatment of 4-methylpyrazole (4-MP), increased cytotoxicity, ROS production, antioxidant enzyme activity, and loss of MMP were observed. The addition of quercetin, catechin, caffeic acid and phytic acid to these cells showed suppression of non-oxidative ethanol metabolism-induced cytotoxicity, similar to oxidative ethanol metabolism. These results suggest that quercetin, catechin, caffeic acid and phytic acid have protective effects against ethanol metabolism-induced oxidative insult in SK-Hep-1 cells by blocking ROS production and elevating antioxidant potentials.

• Biomolecules & Therapeutics
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• 제20권3호
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• pp.352-356
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• 2012

The present study was undertaken to determine whether ethanol influences on the agonist-induced vascular smooth muscle contraction and, if so, to investigate the related mechanism. The measurement of isometric contractions using a computerized data acquisition system was combined with molecular experiments. Ethanol significantly inhibited thromboxane $A_2$ mimetic-induced contraction with intact endothelial function, but there was no relaxation on thromboxane $A_2$ mimetic U-46619-induced contraction irrespective of endothelium suggesting that the pathway such as Rho-kinase activation, $Ca^{2+}$ entry or thin filament regulation was not affected. In addition, ethanol didn't decrease thromboxane $A_2$ mimetic-induced increase of phospho-myosin phosphatase targeting subunit protein 1 (pMYPT1) or pERK1/2. Interestingly, ethanol didn't inhibit significantly phorbol ester-induced contraction in denuded muscles suggesting that thin filament regulation is less important on the ethanol-induced regulation in the muscle than endothelial NO synthesis. In conclusion, this study provides the evidence and possible related mechanism concerning the effect of ethanol on the agonist-dependent contraction in rat aortic rings with regard to endothelial function.

• 한국미생물·생명공학회지
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• 제50권1호
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• pp.157-163
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• 2022

Alcoholic liver disease (ALD), which encompasses alcoholic steatosis, alcoholic hepatitis, and alcoholic cirrhosis, is a major cause of morbidity and mortality worldwide. Although the economic and health impacts of ALD are clear, few advances have been made in its prevention or treatment. We recently demonstrated that the insect-derived antimicrobial peptide CopA3 exerts anti-apoptotic and anti-inflammatory activities in various cell systems, including neuronal cells and colonic epithelial cells. Here, we tested whether CopA3 inhibits ethanol-induced liver injury in mice. Mice were intraperitoneally injected with ethanol only or ethanol plus CopA3 for 24 h and then liver injury and inflammatory responses were measured. Ethanol enhanced the production of proinflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interferon (IFN)-γ, and IL-10. It also induced hepatocyte apoptosis and ballooning degeneration in hepatocytes. Notably, all these effects were eliminated or significantly reduced by CopA3 treatment. Collectively, our findings demonstrate that CopA3 ameliorates ethanol-induced liver cell damage and inflammation, suggesting the therapeutic potential of CopA3 for treating ethanol-induced liver injury.

• 대한한의학회지
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• 제43권3호
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• pp.1-15
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• 2022

Objectives: Myrrh have been used as a traditional remedy to treat infectious and inflammatory diseases. However, it is largely unknown whether myrrh ethanol extract could exhibit the inhibitory activities against particulate matter (PM)-induced skin injury on human keratinocytes, HaCaT cells. Therefore, this study was aimed to investigate the inhibitory activity of myrrh ethanol extract on PM-induced skin injury in HaCaT cells. Methods: To investigate the inhibitory effects of myrrh ethanol extract in HaCaT cells, the skin injury model of HaCaT cells was established under PM treatment. HaCaT keratinocyte cells were pre-treated with myrrh ethanol extract for 1 h, and then stimulated with PM. Then, the cells were harvested to measure the cell viability, reactive oxygen species (ROS), pro-inflammatory cytokines including interleukin (IL) 1-beta, IL-6, and tumor necrosis factor (TNF)-𝛼, hyaluronidase, collagen, MMPs. In addition, we examined the mitogen activated protein kinases (MAPKs) and inhibitory kappa B alpha (I𝜅-B𝛼) as inhibitory mechanisms of myrrh ethanol extract. Results: The treatment of myrrh ethanol extract inhibited the PM-induced cell death and ROS production in HaCaT cells. In addition, myrrh ethanol extract treatment inhibited the PM-induced elevation of IL-1beta, IL-6, and TNF-𝛼. Also, myrrh ethanol extract treatment inhibited the increase of hyaluronidase, MMP and decrease of collagen. Furthermore, myrrh ethanol extract treatment inhibited the activation of MAPKs and the degradation of I𝜅-B𝛼. Conclusions: Our result suggest that treatment of myrrh ethanol extract could inhibit the PM-induced skin injury via deactivation of MAPKs and nuclear factor (NF)-𝜅B in HaCaT cells. This study could suggest that myrrh ethanol extract could be a beneficial agent to prevent skin damage or inflammation.

• Preventive Nutrition and Food Science
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• 제9권3호
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• pp.245-252
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• 2004

This study investigated the effects of an ethanol extract of Allium monanthum MAX. (AME) on ethanol-induced hepatotoxicity in rat liver. Sprague-Dawley rats weighing 100～150 g, were divided into 5 groups; normal group (NOR), AME 200 mg/kg treated group (S1), ethanol (35%, 10 mL/kg) treated group (S2), AME 200 mg/kg and ethanol (35%, 10 mL/kg) treated group (S3) and AME 400 mg/kg and alcohol (35%, 10 mL/kg) treated group (S4). AME was fractionated by the following solvents: n-hexane, chloroform, EtOAC and n-BuOH. Antioxidant index of the n-BuOH fraction was 600 ppm, highest among fractions. The growth rate and feed efficiency ratio were decreased by ethanol, but gradually increased to the corresponding level of the normal group by administering AME. The serum ALT activities that were elevated by ethanol were significantly decreased by AME administration. It was also observed that the hepatic activities of SOD, catalase, xanthine oxidase and GSH-Px that were increased by ethanol were also markedly decreased in the AME treated group with compared to ETB. These results suggest that ethanol extracts of Allium monanthum MAX. may have a protective effect on ethanol-induced hepatotoxicity in rat liver.