• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.10
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• pp.1431-1438
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• 2015

This study was conducted to determine the effects of fermented water extracts from Ligularia fischeri (LAF) on reduction of hepatotoxicity induced by ethanol in rats. Ethanol-treated Sprague-Dawley rats were divided into the following eight groups: ethanol-treated group (control), ethanol and ursodeoxycholic acid-treated group (positive control), ethanol and non-fermented water extracts from Ligularia fischeri (LA)-treated groups [100, 200, and 400 mg/kg BW (body weight)], ethanol and LAF-treated groups (100, 200, and 400 mg/kg BW). ${\gamma}$-Glutamyl transferase activities of the ethanol+LA-treated (100, 200, and 400 mg/kg BW) groups and ethanol+LAF-treated (400 mg/kg BW) group decreased significantly compared to those in the control group (P<0.05). Aspartate aminotransferase activities of the ethanol+LAF-treated (100, 200, and 400 mg/kg BW) groups and ethanol+LA-treated (200 and 400 mg/kg BW) groups decreased significantly compared to those in the control group (P<0.05). Alanine aminotransferase and lactate dehydrogenase activities of all groups significantly decreased compared to those in the control group (P<0.05). The total cholesterol, low density lipoprotein-cholesterol, and triglyceride levels of all groups tended to decrease compared to those in the control group, but the differences were not significant. Superoxide dismutase activity of liver tissues was enhanced in the ethanol+LAF-treated (400 mg/kg BW) group (P<0.05). The contents of malondialdehyde in liver tissues decreased in the ethanol+LAF-treated groups (P<0.05). All treated groups showed well preserved lobular architectures with no evidence of steatosis or liver damage compared to the control group. As the results of this study, LAF may improve the plasma lipid profile and alleviate hepatic damage by ethanol.

• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.8
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• pp.1099-1106
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• 2011

Cucumber fermentation has been used as a means of preservation. This study was performed to investigate the effects of fermented cucumber beverage (CF) containing beneficial materials for an ethanol hangover based on Hovenia dulcis (SKM) on ethanol-induced hepatotoxicity. Male Sprague-Dawley rats were randomly divided into three groups: ethanol control, ethanol plus SKM, and ethanol plus CF+SKM. SKM or CF+SKM was orally administered at a dose of 7 mL/kg body weight once per day for 5 weeks. Control rats were given an equal amount of water. CF+SKM significantly lowered plasma ethanol levels, whereas SKM tended to decrease the levels compared to the control. Both SKM and CF+SKM significantly lowered the plasma acetaldehyde levels and serum transaminase activities compared to those in the control. SKM and CF+SKM did not affect hepatic alcohol dehydrogenase activity; however, it significantly inhibited cytochrome P450 2E1 (CYP2E1) activity. Hepatic aldehyde dehydrogenase (ALDH) activity was significantly higher in the SKM and CF+SKM groups than that in the control group. Plasma acetaldehyde concentration was significantly correlated with hepatic CYP2E1 (r=0.566, p<0.01) activity and ALDH (r=-0.564, p<0.01) activity. Hepatic superoxide dismutase and catalase activities as well as glutathione content increased with the SKM and CF+SKM administration, whereas lipid peroxide content decreased significantly. Furthermore, SKM and CF+SKM lowered plasma and hepatic lipid content and lipid droplets compared to those in the control group. These results indicate that SKM and CF+SKM exhibit hepatoprotective properties partly by inhibiting CYP2E1 activity, enhancing ALDH activity and stimulating the antioxidant defense systems in ethanol-treated rats.

• Journal of Applied Biological Chemistry
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• v.55 no.2
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• pp.85-94
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• 2012

The anti-obese, hypolipidemic and hepatoprotective effects of post-fermented green tea by Monascus pilosus was tested with mice fed with high-fat diet for 7 weeks. The body weight gain and feed efficiency ratio (FER) in normal control group (NC), CHA (2% non-fermented green tea powder supplemented high-fat diet group) and mCHA (2% green tea powder post-fermented by M. pilosus supplemented high fat diet group) groups were significantly lower than those of high fat diet control group (HC). Epididymal fat weight in mCHA and NC were significantly lower than HC. The hepatic lipid peroxide was dramatically higher in HC than that of NC and was significantly lower in CHA and mCHA. In addition, dehydrogenase type activity of xanthine oxidoreductase in HC was lower than that of NC, but significantly higher than CHA and mCHA. In histopathological findings, hepatic fat accumulation in HC was higher than that of NC, CHA and mCHA. Antiobese, hypolipidemic and antifatty liver effect of green tea powder post-fermented by M. pilosus was slightly higher than that of non-fermented green tea. In conclusion, the constituents of green tea fermented by M. pilosus has been proven to not only inhibit obesity and hyperlipidemia but also decrease the hepatic fat accumulation in high fat diet-induced obese mice.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.407-416
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• 1996

The reactive intermediates formed during the metabolism of therapeutic agents, toxicants and carcinogens by cytochromes P450 are frequently capable of covalently binding to tissue macromolecules and causing tissue damage. It has been shown that YH439, a congener of malotilate, is effective in suppressing hepatic P450 2E1 expression. The present study was designed to further establish the mechanistic basis of YH439 protection against toxicant by assessing its effects against chemical-mediated potentiated hepatotoxicity. Retinoyl palmitate (Vit-A) pretreatment of rats for 7 days substantially enhanced carbon tetrachloride hepatotoxicity, as supported by an ${\sim}5-fold$ increase in serum alanine aminotransferase (ALT) activity, as compared to $CCl_4$ treatment alone. The elevation of ALT activity due to Vit-A was completely blocked by the treatment of $GdCl_3$ a selective inhibitor of Kupffer cell activity. Concomitant pretreatment of rats with both YH439 and Vit-A resulted in a 94% decrease in Vit-A-potentiated $CCl_4$ hepatotoxicity. YH439 was also effective against propyl sulfide-potentiated $CCl_4-induced$ hepatotoxicity. Whereas propyl sulfide (50 mg/kg, 7d) enhanced $CCl_4-induced$ hepatotoxicity by >5-fold, relative to $CCl_4$ treatment alone, concomitant treatment of animals with both propyl sulfide and YH439 at the doses of 100 and 200 mg/kg prevented propyl sulfide-potentiated $CCl_4$ hepatotoxicity by 35% and 90%, respectively. Allyl sulfide, a suppressant of hepatic P450 2E1 expression, completely blocked the propyl sulfide-enhanced hepatotoxicity, indicating that propyl sulfide potentiation of $CCl_4$ hepatotoxicity was highly associated with the expression of P450 2E1 and that YH439 blocked the propyl sulfide-enhanced hepatotoxicity through modulation of P450 2E1 levels. Propyl sulfide- and $CCl_4-induced$ stimulation of lipid peroxidation was also suppressed by YH439 in a dose-related manner, as supported by decreases in malonedialdehyde production. The role of P450 2E1 induction in the potentiation of $CCl_4$ toxicity and the effects of YH439 were further evaluated using pyridine as a P450 2E1 inducer. Pyridine pretreatment substantially enhanced the $CCl_4$ hepatotoicity by 23-fold, relative to $CCl_4$ alone. YH439, however, failed to reduce the pyridine-potentiated toxicity, suggesting that the other form(s) of cytochroms P450 inducible by pyridine, but not suppressible by YH439 treatment, may play a role in potentiating $CCl_4-induced$ hepatotoxicity. YH439 was capable of blocking cadmium chloride-induced liver toxicity in mice. These results demonstrated that YH439 efficiently blocks Vit-A-enhanced hepatotoxiciy through Kupffer cell inactivation and that the suppression of P450 2E1 expression by YH439 is highly associated with blocking of propyl sulfide-mediated hepatotoxicity.