• Herbal Formula Science
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• v.28 no.2
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• pp.179-187
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• 2020

Objectives : This study investigated the hepatoprotective effects effects of Jageum-jung extract on alcohol-induced liver disease mice model. Methods : Alcoholic liver disease was induced by Ethanol in C57/BL6 male mice, which were fed Lieber-DeCarli liquid diet containing ethanol. Jageum-jung (100,200 and 300 mg/kg bw/day) were orally administered daily in the alcoholic fatty liver disease mice for 16 days. Results : The results indicate that Jageum-jung promotes hepatoprotective effects by significantly reducing aspartate transaminase (AST) and alanine transaminase (ALT) levels as indicators of liver damage in the serum. Furthermore, Jageum-jung decreased accumulation of triglyceride and total cholesterol, increased levels of superoxide dismutase (SOD) and glutathione (GSH) in the serum of the alcoholic fatty liver disease mice model. Additionally, it improved the serum alcohol dehydrogenase (ADH) activity. Conclusions : This study confirmed the anti-oxidative and hangover elimination effects of Jageum-jung extract, and suggests the possibility of using Jageum-jung to treat alcholic liver disease.

• Journal of Nutrition and Health
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• v.32 no.6
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• pp.628-636
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• 1999

There is a marked increase in geriatric disease, especially liver disease, due to the continuous increase in alcohol and fat consumption. Since the fatty liver, induced by alcohol or fat, is basically from abnormalities in the lipid metabolism, it is possible that fatty acid binding protein(FABP) which is related to the fatty acid metabolism may also be abnormal in these livers. FABP is a small molecular weight protein family present in cytosol in high concentration. It has been proposed as a fatty acid transfer protein and as a binding protein responsible for controlling intracellular free fatty acid concentration. In this research, we have examined the relationship between liver FABP and fatty liver induced by alcohol or high cholesterol diet. Rats were fed one of either semipurified liquid diets; control diet containing 65% carbohydrate, 20% protein, and 15% fat or high cholesterol diet containing 1%(w/w) cholesterol or alcohol diet containing 37% of alcohol instead of carbohydrate. After 5 weeks of feeding period, all rats received commercial chow diet for 5 weeks to examine recovery effect. Liver and blood samples were collected at 0, 1, 3, 5 and 10 weeks to analyze lipid compositions. FABP was purified from liver cytosol and injected to rabbit to obtain antiserum. Liver FABP amount was determined by SDS-PAGE and western blotting methods. Fatty acid binding capacity was determined by binding of 14Cpalmitate with the delipidated liver cytosol. Consumption of alcohol increased serum cholesterol, triglyceride concentration and decreased HDL-cholesterol concentration after 5 weeks. Serum apolipoprotein B concentration increased after 3 weeks and LDL-cholesterol and apolipoprotein A concentration changed after 1 week. Liver cholesterol and triglyceride concentration increased after 3 weeks. Consumption of high cholesterol diet changed liver and serum lipid composition after 3 weeks. Swiching to normal diet for 5 weeks did not normalize most of lipid composition in serum and liver except serum and liver except serum cholesterol, triglyceride and liver cholesterol. Liver cytosol FABP content and the fatty acid binding capacity decreased dramatically after 1 week with alcohol consumption. This results indicate that FABP content changes before the changes before the changes of blood or liver lipid composition, suggesting changes of FABP may cause development of the fatty liver induced by alcohol and can be used as an index of detecting a early development of fatty liver.

• Journal of Microbiology and Biotechnology
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• v.34 no.10
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• pp.2100-2111
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• 2024

Alcoholic liver disease (ALD) poses a significant global health burden, often requiring liver transplantation and resulting in fatalities. Current treatments, like corticosteroids, effectively reduce inflammation but carry significant immunosuppressive risks. This study evaluates Lactiplantibacillus plantarum FB091, a newly isolated probiotic strain, as a safer alternative for ALD treatment. Using an in vivo mouse model, we assessed the effects of L. plantarum FB091 on alcohol-induced liver damage and gut microbiota composition. Alcohol and probiotics administration did not significantly impact water/feed intake or body weight. Histopathological analysis showed that L. plantarum FB091 reduced hepatocellular ballooning and inflammatory cell infiltration in liver tissues and mitigated structural damage in colon tissues, demonstrating protective effects against alcohol-induced damage. Biomarker analysis indicated that L. plantarum FB091 decreased aspartate aminotransferase levels, suggesting reduced liver damage, and increased alcohol dehydrogenase activity, indicating enhanced alcohol metabolism. Additionally, cytokine assays revealed a reduction in pro-inflammatory TNF-α and an increase in anti-inflammatory IL-10 levels in colon tissues of the L. plantarum FB091 group, suggesting an anti- inflammatory effect. Gut microbiota analysis showed changes in the L. plantarum FB091 group, including a reduction in Cyanobacteria and an increase in beneficial bacteria such as Akkermansia and Lactobacillus. These changes correlated with the recovery and protection of liver and colon health. Overall, L. plantarum FB091 shows potential as a therapeutic probiotic for managing ALD through its protective effects on liver and colon tissues, enhancement of alcohol metabolism, and beneficial modulation of gut microbiota. Further clinical studies are warranted to confirm these findings in humans.

• The Journal of Korean Medicine
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• v.18 no.1
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• pp.411-429
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• 1997

Recent survey shows that chronic liver disease such as chronic hepatitis, liver cirrhosis and hepatoma is the third leading causes for death in Korea. In oriental medicine, viral hepatitis is related to Hwangdal(黃疸) and alcoholic liver disease is related to Joosang(酒傷). ARTEMISIAE HERBA and PUERARIAE RADIX have long been used in treating those symptoms. This study was done to evaluate the effect of AR1EMISIAE HERBA and PUERARIAE RADIX on viral and alcoholic hepatitis. ARTEMISIAE HERBA and PUERARIAE RADIX were decocted respectively with water and followed by vaccum evaporation. The solution was diluted to adequate concentration. Sprague-Dawley rats were used in this experiment. Each group was given PUERARIAE RADIX or ARTEMISIAE HERBA solution orally and CCl4, d-galactosamine or alcohol was given orally 30 minutes later. After 24 hours of starvation, blood samples were taken to check serum GOT, GPT, LDH and ALP activities, TC, TG, glucose and BUN levels. These results show that ARTEMISIAE HERBA has better effect on liver injury induced by d-Galactosamine than PUERARIAE RADIX and that both ARTEMISIAE HERBA and PUERARlAE RADIX have good effect on acute alcoholic liver disease while in the liver injury induced by $CCl_{4}$, PUERARIAE RADIX has better inhibitory effect on serum AST, ALT and ALP levels and ARTEMISIAE HERBA has better inhibitory effect on serum total cholesterol and triglyceride. And the result that high concentration group has better effect shows these effects are concentration-dependent. Further study on the mechanism of these herbs is still required.

• Korean Journal of Plant Resources
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• v.36 no.3
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• pp.198-206
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• 2023

The effectiveness of the extracts of Alnus japonica and Portulaca oleracea, which are effective in improving alcohol-induced liver damage, was confirmed using acute and chronic alcoholic liver injury animal models. In the acute alcoholic liver injury model, dieting Alnus japonica and Portulaca oleracea complex (ALPOC) at a dose of 50 mg/kg showed no significant change in liver or body weight, while measured plasma ALT activity to be deficient (28.12 U/ml) compared to the alcohol intake group (42.5 U/ml), and confirmed that restored it to an average level. It showed an improvement of 34.9% compared to the alcohol intake group. AST activity confirmed that it showed a very effective liver protection activity by showing a gain of 12.6%. The chronic alcoholic liver damage animal model demonstrated that ALT showed an improvement effect of 25%, and AST showed an effect similar to that of the positive control group, Hovenia extract. In addition, through H&E staining analysis, observed that the ALPOC improved the necrosis and bleeding of the liver. And the ALPOC group showed intense antioxidant activity of 127% or more compared to the alcohol intake group, and this was confirmed to have a very high activity, which is more than 20% higher than that of the hovenia fruit extract.

• IMMUNE NETWORK
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• v.10 no.6
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• pp.181-187
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• 2010

Excessive alcohol consumption is one of the critical causative factors leading to alcoholic liver disease (ALD). ALD is characterized by a wide spectrum of liver damage, ranging from simple uncomplicated liver steatosis (fatty liver) to steatohepatitis and liver fibrosis/cirrhosis. It has been believed that the obvious underlying cause for ALD is due to hepatocyte death induced by alcohol itself. However, recent sparkling studies have shown that diverse immune responses contribute to ALD because liver is enriched with numerous immune cells. Especially, a line of evidence has suggested that innate immune cells such as Kupffer cells and natural killer (NK)/NKT cells are significantly involved in the pathogenesis of ALD via production of pro-inflammatory cytokines and other mediators. Indeed, more interestingly, hepatic stellate cells (HSCs), known as a major cell inducing liver steatosis and fibrosis, can be killed by liver NK cells, which could be suppressed by chronic alcohol consumption. In this review, with the view of liver as predominant innate immune organ, we describe the pathogenesis of ALD in which what roles of innate immune cells are and how they are interacting with HSCs.

• Journal of Preventive Medicine and Public Health
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• v.38 no.2
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• pp.175-181
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• 2005

Objectives: This study estimated the burden of disease due to high alcohol consumption using DALY, a composite indicator recently developed by the Global Burden of Disease study group. The results were analyzed by age and sex. Methods: Firstly, high alcohol consumption-related diseases, and their relative risk (RR), were selected. Secondly, population attributable fractions (PAFs) were computed using formulae, including the relative risk (RR) and prevalence of exposure (Pe). Thirdly, the DALYs of high alcohol consumption-related diseases were estimated. Lastly, the attributable burdens of diseases due to high alcohol consumption wereconcluded as being the sum of the products that multiplied the DALYs of high alcohol consumption-related diseases by their population attributable fraction (PAF). Results : The burden of high alcohol consumption in Korea was 2992.3 person years (PYs) per 100,000 persons in men, and 1426.6 in women. For men, the high alcohol consumption-induced diseases with the five biggest burdens were liver cirrhosis, hypertensive disease, liver cancer, cerebral infarction and intracerebral hemorrhage. For women, these were cerebral infarction, intracerebral hemorrhage, hypertensive disease, liver cirrhosis and liver cancer. Conclusion: This study highlighted the attributable fraction of diseases due to exposure to high alcohol consumption, by quantifying the results of exposure to risk factors. Therefore, it is now possible to assess interventions for risk factors in quantifiable terms in each population. Finally, measuring the risk factor burdens was expected to contribute to priority setting and effective resource allocation in public health policy.

• Toxicological Research
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• v.14 no.2
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• pp.157-161
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• 1998

The mechanism of active aldehyde-induced liver disease and the enzymatic basis of detoxification were investigated using normal rat liver cell, Ac2F. Aliphatic alcohols including l-decyl alcohol, l-nonanol, l-heptanol, l-hexanol, l-propanol and allyl alcohol exerted a dose- and time-de-pendent toxicity to Ac2F cells. The extent of their toxicities in buthionine sulfoximine (inhibitor of glutathione synthesis) pretreated cells was greater than in pargyline (inhibitor of aldehyde dehydrogenase, ALDH). On the other hand, the toxicity of these alcohols were not affected by 4-methylpyrazole (inhibitor of alcohol dehydrogenase, ADH). These results suggest that the contents of glutathione (GSH) seems to be very important in protecting the cells from toxicants such as aliphatic alcohols.

• Smart Media Journal
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• v.2 no.2
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• pp.33-38
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• 2013

In this paper, we investigated baseline estimation methods for remove background noise using Raman spectra from acute alcohol liver injury and acute ethanol-induced chronic liver fibrosis. Far the baseline estimation, we applied first derivative, linear programming and rolling ball method. Optimal input parameter of each method were determined by the training rate of MAP (maximum a posteriori probability) classifier. According to the experimental results, classification results baseline estimation with the rolling ball algorithm gave about 89.4%, which is very promising results for classification of acute alcohol liver injury and acute ethanol-induced chronic liver fibrosis. From these results, to determined the appropriate methods and parameters of baseline estimation impact on classification performance was confirmed.

• Journal of Convergence Korean Medicine
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• v.5 no.1
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• pp.45-54
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• 2023

Objectives : Alcohol-induced liver disease advances as to reactive oxygen species (ROS) and cellular lipid peroxidation increase. We examined the hepatoprotective effects of Zingiber officinale Roscoe rhizome extract (ZR), Pueraria lobata Ohwi flower extracts (PF), and a newly developed herbal juice (HJ), which was a combination of ZR and PF extracts, against ethanol-induced hepatotoxicity. Methods: The study utilized the human hepatoma cell line HepG2 cells to validate the hepatoprotective effect of HJ (50~200 ㎍/mL) against ethanol (EtOH, 700 mM)-induced liver damage. Results: HJ effectively reduced the protein expression of sterol regulatory element-binding transcription factor 1, adiponectin, and AMP-activated protein kinase in EtOH-induced HepG2 cells. The levels of ROS, total cholesterol, and triglycerides, which are the result of various synthesis and lipogenesis processes induced by EtOH in the liver, were reduced by HJ. Furthermore, the activities of alcohol dehydrogenase and aldehyde dehydrogenase, enzymes linked to alcohol degradation, were more effectively downregulated by HJ treatment compared to treatment with ZR and PF alone, all without causing cytotoxic effects. Conclusions: HJ protects the liver by inhibiting EtOH-induced lipogenesis, lowering ROS generation, and improving alcohol degradation, which is more effective than ZR and PF alone. Further, in vivo experiments can offer additional evidence regarding the effectiveness, safety, and underlying mechanism of action of HJ.