• Korean Journal of Food Science and Technology
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• v.41 no.1
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• pp.93-99
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• 2009

This study aimed to determine whether or not glycoprotein isolated from Cudrania tricuspidata Bureau fruit(CTB glycoprotein) exerts a hepatoprotective effect on liver injury induced by the administration of carbon tetrachloride($CCl_4$, 1.0mL/kg) to A/J mice. Following the administration of CTB glycoprotein(0-20mg/kg), the activities of antioxidant enzymes (superoxide dismutase(SOD), catalase(CAT), and glutathione peroxidase(GPx)), and the quantities of measured thiobarbituric acid reactive substances(TBARS), lactate dehydrogenase(LDH), and nitric oxide(NO) were evaluated from the murine liver tissues and plasma. Additionally, the activity of nuclear factor-kappa B(NF-${\kappa}B$) was assessed after pretreatment with $CCl_4$. When the mice were treated with $CCl_4$ alone, the activities of antioxidative enzymes reduced but amounts of TBARS, LDH, and NO increased. However, the results of treatment with CTB glycoprotein(10 and 20 mg/kg) revealed significantly increased activities of antioxidant enzymes(SOD, CAT, and GPx), as compared with $CCl_4$ alone. On the other hand, the result showed significant diminutions of the quantities of TBARS, LDH, and NO after treatment with CTB glycoprotein(10 and 20 mg/kg), as compared to $CCl_4$ alone. The activity of NF-${\kappa}B$ also declined after pretreatment with CTB glycoprotein, as compared with $CCl_4$ treatment alone. Thus, it is suggested that the CTB glycoprotein exerts a protective effect against $CCl_4$-induced liver injury in A/J mice.

• Korean Journal of Medicinal Crop Science
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• v.18 no.5
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• pp.323-328
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• 2010

Root extract of Lythrum salicaria reported a hepato-protective effect on $CCl_4$-induced liver toxicity of rat was prepared into fractions such as n-hexane up layer (HA), n-hexane down layer (HB), diethyl ether (E), ethylacetate (EA), n-butanol (B) and water (W). Fractions prepared were tested their activities in vitro and in vivo condition. All of the fractions showed effective antioxidant asctivities on DPPH radical and $CuSO_4$-induced oxidation of human low density lipoprotein and E fraction showed the highest inhibitory effect (98.1% at $50\;{\mu}g/m{\ell}$) on linoleic acid autoxidation at $40^{\circ}C$, which was more effective than $\alpha$-tocopherol (82.4%). Five fractions (H = HA plus HB, E, EA, B, and W, 150 mg/kg/day) were fed into Sprague Dawley, male rats for 4 days, which were intoxicated with intra-peritoneal injection of carbon tetrachloride ($1\;m{\ell}/kg$ in corn oil) at the 4th day and were sacrificed in 24 hrs. Serum tumor necrosis factor-alpha (TNF-$\alpha$), a proinflammatory cytokine, elevated with $CCl_4$-intoxication in negative control group ($83\;pg/m{\ell}$) was significantly decreased in E fraction-supplemented group ($18\;pg/m{\ell}$). Cu, Zn-superoxide dismutase (SOD) activity increased in negative control group (0.12 U/mg protein) was decreased in E fraction (0.07 U/mg protein). From the results, it is suggested that ether fraction from root extract of L. salicaria would be a potent antioxidant candidate for ameliorating liver injury induced by chemical intoxicant.

• Journal of Convergence for Information Technology
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• v.11 no.9
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• pp.109-114
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• 2021

Cr(VI)-quinoline compound[(C₉H₇NH)₂Cr₂O₇] was synthesized by the reaction between of quinoline and chromium(VI) trioxide, and structure was FT-IR, elemental analysis. The oxidation ability of benzyl alcohol greatly depends upon the dielectric constant of the used organic solvent, where carbon tetrachloride was worst and N,N'-dimethylformamide was best solvent. Noticeably, in N,N'-dimethylformamide solvent, Cr(VI)-quinoline compound oxidized substituted benzyl alcohols. The Hammett reaction constant(ρ)=-0.69(303K). As a resuit, Cr(VI)-quinoline compound was found as efficicent oxidizing agent that converted benzyl alcohol, allyl alcohol, primary alcohol and secondary alcohols to the corresponding aldehydes or ketones. Cr(VI)-quinoline compound was selective oxidizing agent of benzyl alcohol, allyl alcohol and primary alcohol in the presence of secondary alcohol ones.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.2
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• pp.520-526
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• 2019

The purpose of this experiment is to investigate the feasibility of extracts (sample extract, MSE) mixed with hot - water extracts as health functional nutritional foods for prevention and treatment of liver damage. The experimental method was to investigate the effects of carbon tetrachloride on liver damage in rats by 60% of liver cirrhosis level. The effect of mixed extracts (MSE) was investigated by measuring the physiological functions, biochemical functions, and molecular biologic TGF - ${\beta}$ and P53 levels in liver - injured rats. with MSE doses administered differently(0.50ml, 0.75ml). A total of 30 rats were used for normal group, control group, positive control group, experimental group 1, and experimental group 2. The rats were given 6 times a week for 6 weeks at a fixed time once a day. The results of the experiment were statistically significantly higher in the control group than in the normal group and the positive control group, and statistically significantly lower in the experimental group (1 and 2) than the control group. There were some significant differences in the comparison between the experimental groups (1 and 2), but no significant changes were found. In conclusion, the results of this study are expected to be useful as functional food, and the variation of physiological activity and the degree of liver molecular biotechnology will be used for the research of the same field.

• Journal of Ginseng Research
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• v.47 no.4
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• pp.515-523
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• 2023

Background: 20(S)-protopanaxadiol (PPD), one of the main components of ginseng, has anti-inflammatory, anti-estrogenic, and anti-tumor activities. It is known that activated hepatic stellate cells (HSCs) are the primary producers of extracellular matrix (ECM) in the liver, and the Wnt/β-catenin pathway participates in the activation of HSCs. We aimed to explore whether PPD inhibits liver fibrosis is associated with the Wnt/β-catenin pathway inactivation. Methods: The anti-fibrotic roles of PPD were examined both in vitro and in vivo. We also examined the levels of Wnt inhibitory factor 1 (WIF1), DNA methyltransferase 1 (DNMT1) and WIF1 methylation. Results: PPD obviously ameliorated liver fibrosis in carbon tetrachloride (CCl₄)-treated mice and reduced collagen deposition. PPD also suppressed the activation and proliferation of primary HSCs. Notably, PPD inhibited the Wnt/β-catenin pathway, reduced TCF activity, and increased P-β-catenin and GSK-3β levels. Interestingly, WIF1 was found to mediate the inactivation of the Wnt/β-catenin pathway in PPD-treated HSCs. WIF1 silencing suppressed the inhibitory effects of PPD on HSC activation and also restored α-SMA and type I collagen levels. The downregulation of WIF1 expression was associated with the methylation of its promoter. PPD induced WIF1 demethylation and restored WIF1 expression. Further experiments confirmed that DNMT1 overexpression blocked the effects of PPD on WIF1 expression and demethylation and enhanced HSC activation. Conclusion: PPD up-regulates WIF1 levels and impairs Wnt/β-catenin pathway activation via the downregulation of DNMT1-mediated WIF1 methylation, leading to HSC inactivation. Therefore, PPD may be a promising therapeutic drug for patients with liver fibrosis.

• Journal of Ginseng Research
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• v.47 no.4
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• pp.534-542
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• 2023

Background: Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelial-mesenchymal transition (EMT) plays a key role in the activation of hepatic stellate cells (HSCs). Recently, Rg1 has been shown to reverse liver fibrosis by suppressing EMT, although the mechanism of Rg1-mediated anti-fibrosis effects is still largely unclear. Interestingly, Smad7, a negative regulator of the transforming growth factor β (TGF-β) pathway, is often methylated during liver fibrosis. Whether Smad7 methylation plays a vital role in the effects of Rg1 on liver fibrosis remains unclear. Methods: Anti-fibrosis effects were examined after Rg1 processing in vivo and in vitro. Smad7 expression, Smad7 methylation, and microRNA-152 (miR-152) levels were also analyzed. Results: Rg1 significantly reduced the liver fibrosis caused by carbon tetrachloride, and reduced collagen deposition was also observed. Rg1 also contributed to the suppression of collagenation and HSC reproduction in vitro. Rg1 caused EMT inactivation, reducing Desmin and increasing E-cadherin levels. Notably, the effect of Rg1 on HSC activation was mediated by the TGF-β pathway. Rg1 induced Smad7 expression and demethylation. The over-expression of DNA methyltransferase 1 (DNMT1) blocked the Rg1-mediated inhibition of Smad7 methylation, and miR-152 targeted DNMT1. Further experiments suggested that Rg1 repressed Smad7 methylation via miR-152-mediated DNMT1 inhibition. MiR-152 inhibition reversed the Rg1-induced promotion of Smad7 expression and demethylation. In addition, miR-152 silencing led to the inhibition of the Rg1-induced EMT inactivation. Conclusion: Rg1 inhibits HSC activation by epigenetically modulating Smad7 expression and at least by partly inhibiting EMT.

• Herbal Formula Science
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• v.32 no.1
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• pp.63-82
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• 2024

Objective : Saengkankunbi-tang (SKT) is used as a traditional Korean herbal formula for treatment of liver diseases. We investigated the hepatoprotective effects of SKT plus Epimedium koreanum Nakai (EKE) against arachidonic acid (AA) + iron-mediated cytotoxicity in HepG2 cells and carbon tetrachloride (CCl₄)-mediated acute liver damage in mice. Methods : The cyto-protective effects of SKT + EKE were determined by MTT assay, western blot and fluorescence activated cell sorting analysis. In mice, blood biochemistry and western blot were assessed in CCl₄-induced acute hepatic damage. The animal groups included vehicle-treated control, CCl₄, SKT (200 mg/kg/day), EKE (100 mg/kg/day), SKT (200 mg/kg/day) + EKE (100 mg/kg/day) and silymarin (200 mg/kg/day). Results : In HepG2 cells, pretreatment with SKT + EKE significantly suppressed cytotoxicity induced by AA + iron and reduced the expression of proteins related to apoptosis. In addition, pretreatment with SKT + EKE significantly prevented the increase in H₂O₂ production, GSH depletion, and lower mitochondrial membrane potential induced by AA + iron. In CCl₄-induced liver damage mice, the administration of SKT + EKE prevented the liver damage by inhibition of hepatocyte damage and expression of apoptosis proteins in liver. More importantly, in vitro and in vivo assay, SKT + EKE showed significant effect compare with SKT alone or EKE alone in all parameters. Conclusions : These results indicated that SKT + EKE could protect against oxidative stress-induced liver damage, and SKT + EKE is more effective than SKT alone or EKE alone.

• Journal of Life Science
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• v.18 no.8
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• pp.1053-1058
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• 2008

Glutathione is a well known chemotherapeutic agent for liver disease and is a popular nutritional supplement in the United States. Previous our studies reported the suppressive effects of glutathione-enriched Saccharomyces cerevisiae FF-8 strain (FF-8GY) on carbon tetrachloride- and alcohol-induced hepatotoxicity. The primary objective of this study was to investigate the comparative effects of FF-8GY and commercially available glutathione-enriched yeast extract (GYE) against the oxidative stress in alcohol-induced fatty liver of rats. The lipid peroxidative index (thiobarbituric acid-reactive substances, TBARS) and antioxidant status (reduced glutathione level) were used to monitor those protective roles of FF-8GY or GYE treatment. When the rat was treated alcohol, the TBARS levels in the whole liver and the subfractions of microsomal and mitochondria were significantly increased but these were significantly decreased by FF-8GY treatment and tended to be lowered by GYE treatment. The concentration of hepatic glutathione is known to be closely associated with antioxidant system and this was slightly deplete in the alcohol-induced rats, but this was recovered by treating with FF-8GY. However, the glutathione concentration was more significantly decreased in the GYE supplementation in alcohol feeding rats. Alcohol treatment also negatively affected the serum total protein and albumin, but these were significantly increased near normal levels in FF-8GY coadministered rats. These results suggest that glutathione-enriched Saccharomyces cerevisiae FF-8 strain may have positively mediate the alcohol-induced oxidative stress, and this effect was more pronounced in FF-8GY compared to GYE.

• Applied Biological Chemistry
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• v.49 no.1
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• pp.15-20
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• 2006

EDTA is known to have bacteriocidal effect on Vibrio vulnificus, pathogen of septicemia by osmotic shock in seafoods. Attempts were made to elucidate the bacteriocidal effect of phytic acid (PA) as a substitute for EDTA against V. vulnificus and its inhibition effect on the septicemia, which induces liver damage of the mice by the pathogen. Viable cells of V. vulnificus with the initial titre of $1.7{\times}10^6$ c.f.u. $ml^{-1}$ decreased by 90.6% after 1 min and 99.6% after 5 min in distilled water. The titre decreased by 65.9% and 94.5% in 2 mM solution of $Mg^{2+}$. In 0.1 mM solution of PA, the rate of decrease in titre was 97.4% after 1 min of incubation and 99.8% after 5 min, compared to 95.7% and 99.8% in 0.1 mM solution of EDTA. The bacteriocidal effect of PA solution at a concentration of 1 mM was marked: the rate of decrease in titre was 99.9% after 1 min. In relation to the bacteriocidal effect, PA was evaluated as a potential therapeutic agent for V. vulnificus septicemia in mouse. When the survival periods of mice were investigated by PA and EDTA treatment after the pathogen injection, the group of mice which infected by a low concentration of the strain survived longer than that inoculated at high concentration; also, the ratio of survival was 1.3 times higher in PA than in EDTA, showing that the fatal rate depended on the inoculation concentration. Although survival periods of mice induced with liver damage by carbon tetrachloride and then inoculated with the strain showed a similar trend, the fatal rate of mice was 2 times faster than those inoculated with only pathogen into normal liver, These results indicate that the infection by V. vulnificus was more fatal to those with liver disease. Also, symptoms of hemorrhage and inflammation on the mice with induced liver damage were reduced in case there was phytic acid treatment at each concentration.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.9
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• pp.1344-1349
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• 2005

The aim of this study was to evaluate the effects of Welsh onion administration on $CCl_4$-induced hepatic injury in rats. The increasing rate of the body and organ weight was not significantly different by the ad-ministration of the Welsh onion. Welsh onion (2, 4, $10\%$ w/w) was given for 4 weeks with the injections of $CCl_4$. Total serum lipid was significantly decreased in all treatment groups compared to $CCl_4$ only treatment group (p<0.05). The Welsh onion from winter season was more protective effect by lowering the serum levels of transminase (SGOT and SGPT) compared with others, the levels of transminase - phosphatase (ALP) in serum. The Welsh onion from winter at a dose of $4\%,\;10\%$ (w/w) showed significantly hepatoprotective activity which was comparable to that $CCl_4$-induced hepatic damage. Histological evaluation showed that Welsh onion partially prevented $CCl_4$-induced inflammation, necrosis and vacuolation. Pretreatment of Welsh onion reduced extent of the necrosis found 24 hr after the intraperitoneal administration of $CCl_4$. The present study shows the liver protective action of the Welsh onion against experimentally induced liver damage in rats. This suggests that the Welsh onion may be used as an effective hepatoprotective agent.