• BMB Reports
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• v.44 no.2
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• pp.135-139
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• 2011

Chronic alcohol consumption contributes to numerous diseases, including cancers, cardiovascular diseases, and liver cirrhosis. Epidemiological studies have shown that excessive alcohol consumption is a risk factor for dementia. Along this line, Alzheimer's disease (AD) is the most common form of dementia and is caused by the accumulation of amyloid-$\beta$ ($A{\beta}$ plaques in neurons. In this study, we hypothesized that chronic ethanol consumption is associated with pathological processing of APP in AD. To investigate the relationship between chronic alcohol consumption and $A{\beta}$ production, brain samples from rats fed an alcohol liquid diet for 5 weeks were analyzed. We show that the expression levels of APP, BACE1, and immature nicastrin were increased in the cerebellum, hippocampus, and striatum of the alcohol-fed group compared to the control group. Total nicastrin and PS1 levels were induced in the hippocampus of alcohol-fed rats. These data suggest that the altered expression of APP and $A{\beta}$-producing enzymes possibly contributes to the chronic alcohol consumption-mediated pathogenesis of AD.

• Herbal Formula Science
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• v.28 no.2
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• pp.189-198
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• 2020

Objectives : This study investigated the liver-protective effects of MJY2018, a Herbal formula, against alcoholic fatty liver disease and anti-oxidative effects. Methods : Its effects were investigated in an alcoholic fatty liver disease model in male C57BL/6 mice, which were fed Lieber-DeCarli liquid diet containing ethanol. MJY2018 (100 and 200 mg/kg bw/day) or silymarin (50 mg/kg bw/day) were orally administered daily in the alcoholic fatty liver disease mice for 16 days. Results : The results indicate that MJY2018 promotes hepatoprotection by significantly reducing aspartate transaminase (AST) and alanine transaminase (ALT) levels as indicators of liver damage in the serum. Furthermore, MJY2018 reduced accumulation of triglyceride and total cholesterol, increased levels of superoxide dismutase (SOD) and glutathione (GSH) in the livers of the alcoholic fatty liver disease mice model. Additionally, it improved the serum alcohol dehydrogenase (ADH) activity. Conclusions : These results indicate that MJY2018 were effective in improving and protecting oxidative stress and alcoholic liver disease.

• Journal of Nutrition and Health
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• v.48 no.5
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• pp.390-397
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• 2015

Purpose: In this study, we investigated the effects of chronic alcohol and excessive iron intake on mitochondrial DNA (mtDNA) damage and the progression of alcoholic liver injury in rats. Methods: Twenty-four Sprague-Dawley male rats were divided into four groups (Control, EtOH, Fe, and EtOH + Fe), and fed either control or ethanol (36% of total calories) liquid diet with or without 0.6% carbonyl iron for eight weeks. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, liver malondialdehyde concentrations were measured by colorimetric assays. Liver histopathology was examined by Hematoxylin-eosin staining of the fixed liver tissues. The integrity of the hepatic mtDNA and nuclear DNA was measured by long-range PCR. The gene expression levels of cytochrome c oxidase subunit 1 (Cox1) and NADH dehydrogenase subunit 4 (Nd4) were examined by real-time PCR. Results: Serum ALT and AST activities were significantly higher in the EtOH+Fe group, as compared to the Control group. Similarly, among four groups, liver histology showed the most severe lipid accumulation, inflammation, and necrosis in the EtOH + Fe group. PCR amplification of near-full-length (15.9 kb) mtDNA showed more than 50% loss of full-length product in the liver of the EtOH + Fe group, whereas amounts of PCR products of a nuclear DNA were unaffected. In addition, the changes in the mtDNA integrity showed correlation with reductions in the mRNA levels of mitochondrial gene Cox1 and Nd4. Conclusion: Our data suggested that the liver injury associated with excessive iron and alcohol intake involved mtDNA damage and corresponding mitochondrial dysfunction.

• Food Science of Animal Resources
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• v.31 no.1
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• pp.86-91
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• 2011

This experiment was conducted to investigate the effects of dietary supplementation with lutein-containing materials on meat quality and lutein accumulation in broiler tissue. Broilers were subjected to one of the following treatments: C, basal diet (BD); T1, BD + 2.223% lutein from spinach extracted by ethanol fermentation; T2, BD + 2% radish green powder; T3, BD + 0.61% spinach powder; and T4, BD + 1.83% spinach powder. The weight gain, feed intake, and feed conversion did not differ among treatments. An evaluation of the color of the chicken breast meat revealed that the CIE $L^*$ value of the control was significantly (p<0.05) lower than that of the other treatments, whereas T4 had a significantly (p<0.05) lower CIE $a^*$ value and a higher (p<0.05) CIE $b^*$ value than the other treatments. The lipid oxidation (thiobarbituric acid reaction substances, TBARS) value was not significant among treatments. The results of a high performance liquid chromatography analysis revealed that the lutein peak was present only in the T4 liver tissue. These results showed that spinach powder (T4) affected meat color (CIE $a^*$ and $b^*$) however, TBARS and lutein accumulation were not affected.