• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.7
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• pp.828-834
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• 2006

We investigated whether two-kinds of mixture (NHDT-1 and NHDT-2) mainly composed of Hovenia dulcis Thunb had beneficial actions for alcohol and acetaldehyde degradation in acute alcohol treatment and liver protection from fatty liver induced by chronic alcohol administration. In acute alcohol degradation experiment, serum alcohol and acetaldehyde concentrations exhibited lower 1, 3 and 5 hours after taking 3 g ethanol per kg body weight in NHDT-1 treated rats, but not NHDT-2 including ginseng. On the contrast to the acute effect on alcohol degradation, the long-term alcohol administration revealed that NHDT-2, not NHDT-1, protected the increase in serum concentration of aspartate aminotransferase, alanine aminotrasferase and ${\gamma}-triglyceride$ metabolism similar to the rats not consuming alcohol, leading to decreased triglyceride accumulation in blood and liver. In liver morphological study, NHDT-1 preserved the regular hepatocyte morphology, decreased fat accumulation and reduced sinusoidal leukocyte infiltration in hepatocytes. In conclusion, NHDT-1 plays an important role in alcohol and acetaldehyde degradation without protecting liver damage while NHDT-2 works as hepatocyte protector from alcohol mediated damage.

• Toxicological Research
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• v.11 no.2
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• pp.181-185
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• 1995

To know the mechanism of biphenyl dimethyl dicarboxylate (DDB) in the protection of chemically induced hepatotoxicity, the activity of glutamic pyruvic tran.saminase (GPT) and the level of lipid peroxidation metabolite (malondialdehyde, MDA) and ATP content in hepatocytes were determined in serum and primarily cultured hepatocytes. For in vibo study, rats were pretreated with DDB (300 mg/ kg, p.o.)for 7 days. DDB pretreatment efficiently reduced the elevation of serum GPT activity induced by carbon tetrachloride (1.6 ml/kg, s.c.) and acetaminophen administration (1500 mg/kg, i.p.). In ex vivo study, hepatocytes were isolated from the rats pretreated with DDB (300 mg/kg, p.o.)for 7 days and cultured for 12 hrs before inducing cytotoxicity with chemicals. The MDA formation and the GPT release induced by adriamycin $(1\times10^{-4} mg/ml)$ and cisplatin $(2\times10^{-4} mg/ml)$ were markedly decreased in the hepatocytes from the rats pretreated with DDB as compared to vehicle only. However, DDB pretreatment did not prevent the decrease of ATP contents of hepatocytes induced by cisplatin and adriamycin. In in vitro experiment, DDB was pretreated in primary cultured hepatocytes for 3 days. DDB enhanced the decreases of ATP contents induced by cisplatin and adriamycln. These results suggest that DDB may protect the hepatocytes from injury induced by hepatotoxlcants through inhibiting the lipid peroxidation.

• The Korean Journal of Food And Nutrition
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• v.32 no.4
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• pp.275-283
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• 2019

This study was carried out to investigate the various roles and effects of Morinda citrifolia L.(noni) on the human body and to utilize the findings obtained for future disease related research on food and nutrition. Morinda citrifolia L. has been used in folk medicine by Polynesians for over 2,000 years and is reported to have a broad range of therapeutic effects. Noni is an alkaloid system such as proxeronine, scopoletin, octanoic acid, terpenoids, alkaloids, anthraquinones, nordamnacanthal, morindone, rubiadin, b-sitosterol, flavone glycosides, linoleic acid, acubin, L-asperuloside, caproic acid, caprylic acid, ursolic acid, rutin. Noni's side effects have been reported to affect anti-inflammatory, analgesics, LDL antioxidant, anti-tumor, antifungal, antibiotic, antiviral, antiparasitic and immunosuppressive effects. In particular, noni's efficacy is considered to be important for the prevention of diseases by inhibiting active oxygen, which is a direct cause of oxidative stress, through various metabolites through 'xeronine system'. Noni's functions and effects that have been examined in this study include anti-inflammation, pain relief, antioxidant, anticancer, hepatocyte protection among others. Therefore, noni's extracts are considered highly useful for diverse scientific and nutritional health functional foods.

• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.8
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• pp.1246-1251
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• 2004

To investigate the effects of plant extracts on the protection against liver damage by $CCl_4$ in rat, two kinds of experiment were performed, firstly by the primary hepatocyte culture and secondly by the animal feeding. The primary hepatocyte culture with the extracts of pine leaf, soybean sprout and mugwort showed significantly low activities (p<0.01∼0.05) of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), indicating an excellent protective effect against liver damage by $CCl_4$. In the second experiment, the microsomal malondialdehyde (MDA) contents of the above same groups were also significantly lower (p<0.01) than the $CCl_4$-treated group without plant extracts, but shiitake showed less effect. Among four kinds of plant extracts, extracts of pine leaf and mugwort showed also much higher activities of the microsomal cytochrome P-450 in comparison to soybean sprout and shiitake. In the test of xanthine oxidase (XOD) activity, all of three groups except shiitake showed significantly low activities (p<0.01). These consistent results in vitro and in vivo suggest that the extracts of pine leaf, soybean sprout and mugwort may have strong protective effects against liver damage induced by the potential toxicants such as $CCl_4$.

• International Journal of Industrial Entomology and Biomaterials
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• v.2 no.1
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• pp.15-18
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• 2001

Silk fibroin (SF) derided from the domestic silk worm, bombyx mori, is the natural protein and widely used as bio-functional materials as well as apparels. We studied the livers protective effect of SF from alcohol-induced hepatotoxicity in the alcohol preference mouse. To increase more absorption of SF in experimental animals, molecular weight of SF was lowered by 2N of HCI aqueous solution at 10$0^{\circ}C$ for 48 hrs. SF was added to liquid diet with alcohol and fed to the alcohol preference mice for 4 weeks. To assess the liver function, the concentration of alanine aminotransferase (AlT), aspartate aminotransferase (AST) and cholesterol present in either blood or liver tissue were measured. As compared with non-SF treated groups the SF-treated showed significantly low concentrations of ALT, AST, cholesterol and triacylglycerol values, respectively. Histopathological examination revealed that the extent of hepatocyte injury in the SF-treated group was reduced when it was compared with non SF-treated group. These results suggest that SF may have liver protective effects against alcohol-induced hepatotoxicity.

• Herbal Formula Science
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• v.28 no.4
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• pp.327-337
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• 2020

Objective : Citri Unshius Pericarpium is the dried peel of mature fruit of Citrus unshiu Markovich and has been used to treat indigestion, vomiting, and removal of phlegm. This study investigated the hepatoprotective and antioxidant effect of CEE (Ethanol extract of Citri Unshius Pericarpium) in cadmium (CdCl₂)-treated HepG2 cells. Methods : Component analysis of Citri Unshius Pericarpium was analyzed by UPLC with C₁₈ column. Cell viability was determined by MTT assay. The enzyme activity of superoxide dismutase (SOD) and the level of reactive oxygen species (ROS) and reduced glutathione (GSH) were analyzed using commercially available kits. Results : Cadmium caused severe HepG2 cell death. Cadmium also increased ROS production, consistent with depletion of GSH and inhibition of the SOD enzyme. However, CEE treatment reduced cell death and relieved oxidative stress caused by cadmium toxicity. CEE lowered ROS levels and improved depletion of GSH levels. CEE also enhanced the enzymatic activity of SOD. In component analysis, hesperidin was the most abundant of the five marker compounds (Narigenin, Narigin, Narirutin, Hesperidin and Hesperidin), which assumes that hesperidin partially contributed to the antioxidant activity of CEE. Conclusion : These results suggested that CEE could be a potential substance to solve heavy metal-related health problems. In particular, inhibition of oxidative stress by CEE can be a way to treat liver damage caused by cadmium.

• Herbal Formula Science
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• v.31 no.2
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• pp.111-124
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• 2023

Objectives : Oxidative stress is an important cause of many diseases including liver injury. Therefore, adequate regulation of oxidative stress plays a pivotal role in maintaining liver function. Until recently, there has been no studies on the hepatoprotective effect of Samchulgeonbi-tang (SCGBT). Therefore, the hepatoprotective effect of SCGBT was investigated in HepG2 cells. In this study, oxidative stress was induced by arachidonic acid (AA) and iron. Methods : To analyze the hepatoprotective effects of SCGBT against oxidative stress induced by AA + iron, the cell viability, apoptosis-related proteins and intracellular ROS, glutathione (GSH), and mitochondrial membrane permeability (MMP) were measured. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) transcription activation and expressions of Nrf2 target gene were analyzed through immunoblot analysis. Results : SCGBT increased the cell viability from AA + iron - induced cell death and inhibited apoptosis by regulating apoptosis related proteins. SCGBT protected cells by inhibiting ROS production, GSH depletion, and MMP degradation against AA + iron induced oxidative stress. Furthermore, Nrf2 activation was increased by SCGBT, and the Nrf2 target genes were also activated by SCGBT. Conclusions : These results suggest that the SCGBT has a hepatocyte protection effect and antioxidant effect from AA + iron induced oxidative stress.

• KSBB Journal
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• v.18 no.4
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• pp.329-334
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• 2003

The present study was aimed at investigating the regulatory mechanism in tissue-specific expression of insulin-like growth factor-I (IGF-I) gene. The expression of IGF-I gene was determined by a solution hybridization/RNase protection assay using total RNA prepared from rat liver or brain of various ages. The levels of IGF-I transcripts were increased in liver gradually after birth, but decreased in brain. By using an oligonucleotide (FRE) corresponding to the C/EBP binding site of the rat IGF-I exon 1, multiple forms of C/EBP${\alpha}$ and C/EBP${\beta}$ proteins, which have DNA-binding activity, were detected in the rat liver or brain. Western immunoblot and southwestern analyses show that p42$\^$C/EBP${\alpha}$/, p38$\^$C/EBP${\alpha}$/, p35$\^$C/EBP${\alpha}$/, p38$\^$C/EBP${\beta}$/, and p35$\^$C/EBP${\beta}$ form specific complexes with the IGF-I exon 1 oligonucleotide in liver nuclear extract and that p42$\^$C/EBP${\alpha}$/ and p38$\^$C/EBP${\beta}$/ form complexes in brain. These data suggest that the formation of FRE-C/EBP isoform complexes may play important roles in the tissue-specific regulation of IGF-I gene expression.

• Journal of Physiology & Pathology in Korean Medicine
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• v.29 no.1
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• pp.18-26
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• 2015

Akebiae Caulis is a galenical originated from Akebia quinata Decaisne species. It is commonly used in the treatment of oposiuria, inflammation, nociceptive and fever. Here, we investigated the effect of Akebiae Caulis extract (ACE) to protect hepatocyte against the malfunction of mitochondria and apoptosis. Arachidonic acid (AA)+iron promoted excessive reactive oxygen species (ROS) production and exerted a deleterious effect on mitochondria. Treatment with ACE protected hepatocytes from AA+iron-induced cytotoxicity, as shown by alterations in the protein levels related with apoptosis such as poly(ADP-ribose) polymerase, pro-caspase 3, Bcl-XL and Bcl-2. Moreover, AA+iron-induced $H_2O_2$ production, GSH depletion and mitochondrial dysfunction were alleviated by ACE pretreatment. As a potential molecular mechanism for the ACE-mediated cytoprotection, phosphorylation of AMP-activated protein kinase (AMPK), a key regulator in determining cell survival or death, was increased by ACE. Moreover, ACE treatment enhanced inactive phosphorylation of glycogen synthase kinase-$3{\beta}$ ($GSK3{\beta}$), downstream substrate kinase of AMPK. More importantly, ACE prevented a decrease in the $GSK3{\beta}$ phosphorylation derived by AA+iron, which might contribute to mitohondiral protection and cell survival. To further identify essential compounds in Akebiae Caulis for the protection of AA+iron-mediated cytotoxicity, we found that betulin in combination with hederagenin protected from AA+iron-induced mitochondrial dysfunction. Betulin+hederagenin treatment also increased inactive phosphorylation of $GSK3{\beta}$ in common with ACE. These results suggest that ACE protected hepatocytes against oxidative stress and mitochondrial dysfunction, which is mediated with inactive $GSK3{\beta}$ phosphorylation downstream of AMPK.

• IMMUNE NETWORK
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• v.1 no.3
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• pp.213-220
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• 2001

Background: A previous study has shown that Euonymus alatus (EA) has an antidotic activities against inflammation, suggesting possibility that EA can exert this beneficial effects to liver injury by an initial protection against drug-induced hepatocyte demage. The present study was undertaken to evaluate the protective effect of EA-extract on experimentally induced hepatitis in ICR mice and to investigate some mechanisms responsible for its action. Methods: Water EA extract was used in this experiments. The mice received i.p. a dose of 700 mg/kg galactosamine (GalN) together with $5{\mu}g/kg$ of endotoxin (LPS), or received i.v. 12 mg/kg of concanavalin A (Con A). EA (4 mg/mouse) was administrated on day -2, -1 and 0 before induction of liver injury. Liver injury was assessed by measurement of serum alanin amino-transferase (SGPT) levels on 9 hr after GaIN.LPS, or 8 hr after con A administration. Results: Treatment with either GaIN or LPS alone did not cause hepatitis. However, simultaneous administration of GalN and LPS to mice resulted in LPS-dose dependent fulminant hepatitis. GaLN/LPS-induced liver injury was reduced when mice were given EA for 3 days before induction. This preventive effect of Ea was more prominent when EA was given by intraperitoneal route rather then by oral route. Pretreatment of EA or dexamethasone inhibited significantly $TNF{\alpha}$ production in GalL/LPS-injured mice. However, EA-treatment did not influence $TNF{\alpha}$-induced hepatitis in GalN-sensitized mice, suggesting that $TNF{\alpha}$ is likely to act as one of final mediators of endotoxin action and the protective effect of EA might be manifested chiefly by inhibition of endotoxin-induced $TNF{\alpha}$ production, not by blocking the $TNF{\alpha}$-action. Injection of Con A into mice evoked remarkable liver injury in a dose dependent fashion. This liver damage was reduced by EA-pretreatment. Dexamethasone significantly reduced both GalL/LPS-induced and Con A-induced liver damages, showing synergism with EA. However, indomethacin reduced only GalN/ LPS-induced hepatitis, not for Con A-induced hepatitis. Conclusion: These results led to the conclusion that EA may be able to contribute at least in part to prevent the drug-induced hepatotoxicity, and that its anti-hepatitis effects might be manifested directly by modulation of endogenous mediators, such as leukotriese D4, $TNF{\alpha}$ and free radical, and indirectly by regulation of immune mediated responses. Also these results suggested that EA could be developed as a potential antidotic agent.