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Protective Effects of Ecklonia stolonifera Extract on Ethanol-Induced Fatty Liver in Rats
방채영,변재혁,최혜경,최재수,정세영 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.6
Chronic alcohol consumption causes alcoholic liver disease, which is associated with the initiation of dysregulated lipid metabolism. Recent evidences suggest that dysregulated cholesterol metabolism plays an important role in the pathogenesis of alcoholic fatty liver disease. Ecklonia stolonifera (ES), a perennial brown marine alga that belongs to the family Laminariaceae, is rich in phlorotannins. Many studies have indicated that ES has extensive pharmacological effects, such as antioxidative, hepatoprotective, and antiinflammatory effects. However, only a few studies have investigated the protective effect of ES in alcoholic fatty liver. Male Sprague-Dawley rats were randomly divided into normal diet (ND) (fed a normal diet for 10 weeks) and ethanol diet (ED) groups. Rats in the ED group were fed a Lieber-DeCarli liquid diet (containing 5% ethanol) for 10 weeks and administered ES extract (50, 100, or 200 mg/kg/day), silymarin (100 mg/kg/day), or no treatment for 4 weeks. Each treatment group comprised of eight rats. The supplementation with ES resulted in decreased serum levels of triglycerides (TGs), total cholesterol, alanine aminotransferase, and aspartate aminotransferase. In addition, there were decreases in hepatic lipid and malondialdehyde levels. Changes in liver histology, as analyzed by Oil Red O staining, showed that the ES treatment suppressed adipogenesis. In addition, the ES treatment increased the expression of fatty acid oxidation-related genes (e.g., PPAR-α and CPT-1) but decreased the expression of SREBP 1, which is a TG synthesis-related gene. These results suggest that ES extract may be useful in preventing fatty acid oxidation and reducing lipogenesis in ethanol-induced fatty liver.
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방채영,원은경,박권우,이광원,정세영,Bang, Chae-Young,Won, Eun-Kyung,Park, Kuen-Woo,Lee, Gwang-Won,Choung, Se-Young 대한약학회 2008 약학회지 Vol.52 No.5
In this study we investigated antioxidant activity of against several free radicals and skin whitening effect of 70% ethanol extract (leaf extracts and branch/stem mixed) of Lindera obtusiloba BL. Antioxidant activity was assessed by DPPH, superoxide radical and hydroxyl radical assays. The Lindera obtusiloba BL. extract had antioxidant activity dose dependently with an ${IC}_{50}$ value of 243.14 and 181.10 ${\mu}g$/ml for DPPH, 165.77 and >1500 ${\mu}g$/ml for non-enzymatic system of superoxide radical assay, 35.47 and >100 ${\mu}g$/ml for enzymatic system of superoxide radical assay, 1.21 mg/ml for hydroxyl radical assay. In addition we tested tyrosinase inhibition activity and melanin contents on B16 melanoma F10. B16 melanoma cell was treated by such sample as 1, 5, 10 and 50 ${\mu}g$/ml for 72 hr and tyrosinase inhibition was tested. Melanogenesis was inhibited to 22% at the dose of 50 ${\mu}g$/ml and tyrosinase was inhibited to 45.2% at the same dose. In conclusion Lindera obtusiloba BL had potent antioxidant activity and inhibitory activity of tyrosinase and melanin formation. It could be developed as the health functional food and functional cosmetic resources.
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강보승,방채영,정세영,최경우,최혁중,김창선,예진허치슨 대한결핵 및 호흡기학회 2015 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.120 No.-
Background: Aldehyde dehydrogenase (ALDH) metabolizes acetaldehyde, the major cause of alcohol hangover symptoms. It also detoxifies cytotoxic reactive aldehydes. Influenza virus-induced oxidative stress promotes lipid peroxidation of cellular membrane, leading to the accumulation of reactive aldehydes that contribute to lung injuries. A variety of anti-hangover products are commercially available, however, almost none of them has been proven to show enhanced metabolizing capacity of ALDH in a live subject. We aimed to test a specific product of interest. Methods: A powder sample of anti-hangover (KISLip, Pico Entech, Korea) was examined by in vitro & in vivo experiments to measure the amount of NADH formation which is generated through catalytic conversion of acetaldehyde. In-vivo examination tested the ethanol and acetaldehyde level in blood of rats with oral infusion of substance before or after ethanol intake. Results: The activities of alcohol dehydrogenase & aldehyde dehydrogenase within the anti-hangover substance were 1.84 unit/g and 0.28 unit/g, respectively. The oxidation capacities of rats were dose-dependently increased after substance gavages. Particularly, the cases with oral intake of substance 220 mg/kg after 1hr of ethanol intake have shown more meaningful decreases in acetaldehyde level in blood. Conclusions: Oral intake of anti-hangover substance has significantly enhanced acetaldehyde-metabolizing capacity in rat model, potentially suggesting increased ALDH capacity within circulation and detoxifying ability of other reactive aldehydes.
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Anti-Obesity Effects of Aster spathulifolius Extract in High-Fat Diet-Induced Obese Rats
김사직,방채영,Yuan-Ri Guo,정세영 한국식품영양과학회 2016 Journal of medicinal food Vol.19 No.4
The aim of this study was to investigate the anti-obesity and antihyperlipidemic efficacy and molecular mechanisms of Aster spathulifolius Maxim extract (ASE) in rats with high-fat diet (HFD)-induced obesity. Rats were separately fed a normal diet or a HFD for 8 weeks, then they were treated with ASE (62.5, 125, or 250 mg/kg) for another 4.5 weeks. The ASE supplementation significantly lowered body weight gain, visceral fat pad weights, serum lipid levels, as well as hepatic lipid levels in HFD-induced obese rats. Histological analysis showed that the ASE-treated group showed lowered numbers of lipid droplets and smaller size of adipocytes compared to the HFD group. To understand the mechanism of action of ASE, the expression of genes and proteins involved in obesity were measured in liver and skeletal muscle. The expression of fatty acid oxidation and thermogenesis-related genes (e.g., PPAR-α, ACO, CPT1, UCP2, and UCP3) of HFD-induced obese rats were increased by ASE treatment. On the other hand, ASE treatment resulted in decreased expression of fat intake-related gene ACC2 and lipogenesis-related genes (e.g., SREBP-1c, ACC1, FAS, SCD1, GPATR, AGPAT, and DGAT). Furthermore, ASE treatment increased the level of phosphorylated AMPKα in obese rats. Similarly, the level of phosphorylated ACC, a target protein of AMPKα in ASE groups, was increased by ASE treatment compared with the HFD group. These results suggest that ASE attenuated visceral fat accumulation and improved hyperlipidemia in HFD-induced obese rats by increasing lipid metabolism through the regulation of AMPK activity and the expression of genes and proteins involved in lipolysis and lipogenesis.
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