• Journal of Acupuncture Research
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• v.22 no.5
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• pp.151-160
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• 2005

Objectives : This study was undertaken to examine whether Juglandis Semen herbal acupuncture (JGA) exerts protective effect against oxidant-induced cell injury in rabbit liver. Methods : The cell damage was estimated by measuring lactate dehydrogenase (LDH) release, and lipid peroxidation was estimated by measuring malondialdehyde (MDA) in rabbit liver slices. Results : t-Butylhydroperoxide (tBHP) caused an increase in LDH release and lipid peroxidation in a dose-dependent manner over concentrations of 0.5-2 mM, which were prevented by addition of 0.05% JGA. The protective effect of JGA was dose-dependent in concentration range of 0.005 to 0.1%. The concentrations of 0.005 and 0.1% JGA completely prevented the LDH release and lipid peroxidation by 1 mM tBHP. When liver tissues were exposed to 1 mM tBHP, alanine aminotransferase (ALT) activity in the medium was significantly increased, which was prevented by 0.05% JGA. tBHP (2 mM) decreased GSH content and the effect was prevented by 0.05% JGA. Conclusion : These results suggest that JGA exerts protective effect against oxidant-induced cell injury by antioxidant action resulting from enhancement of GSH content in the liver.

• The Journal of Internal Korean Medicine
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• v.32 no.4
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• pp.550-564
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• 2011

Objectives : Oxidative stress seems to play a major role in mechanisms by which ethanol causes liver injury. Previous studies have shown that treatment with Yinjinchunggan-tang (Yinchenqinggan-tang, YJCGT) has protective effects on alcoholic liver disease. The aim of this study was to investigate the protective effects of YJCGT on alcohol-induced oxidative stress. Materials and Methods : In vitro, we evaluated the inhibitory activities of YJCHT on DPPH(1,1-diphenyl-2-picryl-hydrazyl), xanthine oxidase, trypsin, and hyaluronidase. In a cell culture model, we measured cell viability and proliferation, and the activities of superoxide dismutase (SOD), and catalase (CAT) after YJCGT treatment in C34 and E47 cell lines, and HepG2 cells transfected with/ without cytochrome P450IIE1 (CYP2E1) gene. In vivo, we estimated serum level of hepatic biochemical markers, and alcohol concentration in the blood. Results : YJCGT showed significant free radical scavenging activity against DPPH and xanthine oxidase and decreased hyaluronidase activity effectively in vitro. YJCGT also increased cell viability, and proliferation in C34 and in E47 cell lines, and increased activities of superoxide dismutase, and catalase in C34 and in E47 cell lines. YJCGT reduced serum AST, LDH, and total cholesterol level in some of the results, and reduced blood alcohol concentration in vivo, as well. Conclusions : This study suggests that YJCGT has protective effects on oxidative stress by inhibiting alcohol-induced suppression of antioxidant enzyme activities.

• Environmental Analysis Health and Toxicology
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• v.23 no.4
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• pp.325-335
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• 2008

The protective effects of the Naringin, on carbon tetrachloride ($CCl_4$)-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with Naringin prior to the administration of $CCl_4$ significantly prevented an increase in serum alanine, aspartate aminotransferase activity and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with Naringin also significantly prevented the depletion of glutathione (GSH) content in the livers of $CCl_4$-induced mice. However, reduced hepatic glutathione levels was unaffected by treatment with Naringin alone. In addition, Naringin prevented $CCl_4$-induced apoptosis and necrosis, as indicated by a liver DNA laddering. To determine whether caspase-8,-3 pathway involved in $CCl_4$-induced acute liver injury, caspase-8, -3 activities were tested by ELISA. Naringin attenuated $CCl_4$induced caspase-8, -3 activities in mouse livers. $CCl_4$-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic study. The effects of Naringin on the cytochrome P450 (CYP) 2E1, the major isozyme involved in $CCl_4$ were also investigated. Treatment of mice with Naringin resulted in a significant decrease of the CYP2E1-dependent hydroxyl at ion and aniline in a dose-dependent manner. These findings suggest that protective effects of Naringin against the $CCl_4$-induced hepatotoxicity may be due to its ability to block CYP2E1-mediated $CCl_4$ bioactivation and that is also protects against caspase-8, -3 pathway mediated apoptosis.

• The Journal of Internal Korean Medicine
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• v.29 no.1
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• pp.200-218
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• 2008

Objectives : The purpose of this study was to investigate the effects of Injinchunggan-tang (Yinchenchinggan-tang) on DMN-induced liver damage by applying proteomics. Materials and Methods : Sprague-Dawley rats were used in this experiment and were divided into the normal group (normal saline), the control group (DMN) and the sample group (DMN+IJCGT). DMN was injected i.p. once a day three times a week for 3 weeks in the control group. Normal saline instead of DMN was administered to the normal group. In the sample group, Injinchunggan-tang (Yinchenchinggan-tang) extract was orally administered once a day for 10 days after DMN was induced. The livers of each group were processed and analyzed by histology, Western blot, $Oxyblot^{TM}$, CBB and 2-dimensional electrophoresis. Results : In the histological findings of the liver, IJCGT reduced collagen deposition and liver damage in DMN-induced hepatic fibrosis. IJCGT increased MMP-13 protein production assessed by western blot. Protein oxidation induced by DMN treatment was decreased by IJCGT. In the 2-dimensional electrophoresis finding, the level of the increased proteins induced by DMN treatment such as GRP 75, 58kDa glucose regulated protein and heat shock 70kDa protein 5 were decreased by IJCGT. IJCGT was considered to have the protective effects on hepatotoxicity induced by DMN. In the 2-dimensional electrophoresis finding, the level of increased oxidized proteins such as heat shock 70 protein, mitochondrial malonyltransferase, calreticulin precursor, actin, NADP-isocitrate dehydrogenase, ankyrin repeat and SOCS box protein 11 were decreased by IJCGT. IJCGT was considered to have protective effect on the protein production induced by DMN treatment. Conclusion : Injinchunggan-tang (Yinchenchinggan-tang) exerts an inhibitory effect against the fibrosis and protein oxidation induced by DMN treatment in the rat liver. IJCGT was considered to have protective effects on the hepatotoxicity and protein production induced by DMN treatment.

• The Journal of Internal Korean Medicine
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• v.20 no.1
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• pp.181-197
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• 1999

In order to investigate the protective effect of Samduhaejungtang-gamibang on the liver injury of rats induced by $CCl_4$ and d-galactosamine, the serum transaminase(GOT& GPT) alkaline phosphatase(ALP), lactic dehydrogenase(LDH) for enzyme activities and triglyceride, total bilirubin amounts for serum component were measured. All animals were divided into 4 groups, those were normal group(untreated), control group(treated with vehicle 0.9% Saline solution), sample Ⅰ group(1500mg/kg administrated), sample Ⅱ group(3000mg/kg administrated). The results were as follows: 1. The inhibitory effects of the serum GOT activities in rats induced by $CCl_4$ were noted in sample Ⅱ group(p<0.01). In serum GPT activities, sample Ⅱ group(p<0.05) only showed the inhibitory effects. 2. The inhibitory effects of the serum ALP activities in rats induced by $CCl_4$ were noted in sample Ⅱ group(p<0.01) 3. The inhibitory effects of the serum LPH activities in rats induced by $CCl_4$ were noted in sample Ⅱ group, but it is not recognized statistically. 4. The increases effects of the serum triglyceride content level in rats induced by $CCl_4$ were inhibited in both sample Ⅰ group(p<0.05) and sample Ⅱ group(p<0.01) 5. The increases effects of the serum total bilirubin content level in rats induced by $CCl_4$ were inhibited in sample Ⅱ group(p<0.05) 6. The inhibitory effects of the serum GOT, GPT activities in rats induced by d-galactosamine were noted in sample Ⅱ group (p<0.001), but sample Ⅰ group was not recognized. 7. The signiticantly inhibitory effects of in the serum LDH activities in rats induced by d-galactosamine were noted in both sample Ⅰ group(p<0.05) and sample Ⅱ group (p<0.001) 8. The increases of the serum ALP content level in rats induced by d-galactosamine were inhibited in sample Ⅱ group(p<0.05) 9. The increases of the serum total bilirubin content level in rats induced d-galactosamine were inhibited in sample Ⅱgroup(p<0.05) According to the above results, it is considered that Samduhaejungtang-gamibang has protective effect against liver injury in rats induced by $CCl_4$ and d-galactosamine. So it is required to study about the actions of mutual relation of medicines and patho-mechanism by experiment.

• 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.

• Preventive Nutrition and Food Science
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• v.8 no.2
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• pp.130-136
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• 2003

The protective effects of onion extract (OE), onion powder extracted in ethanol for 2 days. on carbon tetrachloride ($CCl_4$)-induced hepatotoxicities and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with OE prior to the administration of $CCl_4$ significantly reduced the increase in serum alanine and aspartate aminotransferase activities and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with OE significantly prevented the depletion of reduced glutathione content in the liver of $CCl_4$-intoxicated mice. $CCl_4$-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic findings. The effects of OE on the cytochrome P450 (P450) 2E1, the major isozyme involved in $CCl_4$ biotransformation were investigated. Treatment of mice with OE resulted in a significant decrease in P450 2E1-dependent p-nitrophenol and aniline hydroxylation in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. OE also exhibited antioxidant effects in FeCl$_2$-ascorbate induced lipid peroxidation in rat liver homogenates and in superoxide radical scavenging activity. These results show that the protective effects of OE against the $CCl_4$-induced hepatotoxicity may be due to its ability to block bioactivation of $CCl_4$, mainly tty inhibiting the expression and activities of P450 2E1 and by scavenging free radicals.

• The Journal of Internal Korean Medicine
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• v.31 no.1
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• pp.11-24
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• 2010

Objectives : This study was carried out to investigate the hepatoprotective effects of mixture with Hovenia dulcis Thunb (HDT) and Acer tegmentosum Maxim(ATM) on D-galactosamine-induced liver failure in rats. Methods : The animals were divided into 4 groups: control, with liver failure and no treatment; H1A1, with liver failure and oral treatment with HDT 1 and ATM 1; H1A2, with liver failure and oral treatment with HDT 1 and ATM 2; H1A4, with liver failure and oral treatment with HDT 1 and ATM 4. The animals were treated for 3 weeks and then examinations of change of body weight, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transpeptidase ($\gamma$-GTP), total cholesterol, triglyceride, total bilirubin, superoxide dismutase (SOD), catalase, histopathologic change, and complete blood count (CBC) were performed. Results : All experimental groups had significantly decreased AST in serum and markedly increased activity of SOD as compared with the control group. H1A1, and H1A4 significantly decreased ALT in serum and H1A4 at 2 weeks was significantly higher on the change of body weight as compared with the control group. In histopathologic change of liver tissue by light microscopy, all experimental groups showed recovery effects of liver cells which were damaged by D-galactosamine. Conclusions : Based upon these results, it could be assumed that a mixture of HDT and ATM has hepatoprotective and antioxidative effects on D-galactosamine-induced liver failure. Therefore, a mixture of HDT and ATM might be utilized as a protective agent in therapy for liver diseases.

• YAKHAK HOEJI
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• v.56 no.2
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• pp.99-107
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• 2012

The protective effect of AI-1367 (Alnus japonica extract) on liver injury was investigated. Primary rat hepatocyte intoxication was induced by tert-butyl hydroperoxide (tBH), carbon tetrachloride ($CCl_4$), or D-glactosamine (D-GalN). Liver injury was induced by $CCl_4$, D-GalN or MCD (methionine choline deficient)-diet in mouse. The cellular leakage of lactate dehyrogenase and cell viability followed by the treatment of hepatotoxicants were significantly improved by AI-1367 treatment at a concentration range of 5~50 ${\mu}g/ml$ for tBH, 5~50 ${\mu}g/ml$ for D-GalN, and 5~100 ${\mu}g/ml$ for $CCl_4$, respectively. Treatment with AI-1367 (20, 10, 5 mg/kg, p.o.) on liver injury induced by subcutaneous injection of $CCl_4$ or D-GalN reduced significantly the levels of aspartate transaminase and alanine transaminase in serum. Histological observations revealed that fatty acid changes, hepatocyte necrosis and inflammatory cell infiltration in $CCl_4$ (D-GalN)-induced liver injury was improved by administration of AI-1367. AI-1367 treatment (10, 5, 2.5 mg/kg, p.o.) also significantly recovered the body weight change and serum levels of aspartate transaminase, alanine transaminase and triglyceride in liver injury induced by MCD diet. From these results, AI-1367 shows protective effects against tBH, $CCl_4$, D-GalN, or MCD diet-induced hepatotoxicity in vitro or in vivo.

• Korean Journal of Food Science and Technology
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• v.46 no.2
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• pp.219-223
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• 2014

The purpose of this study was to investigate the protective effects of fucoidan on acute alcohol-induced liver injury in rats. Experimental animals were randomly divided into four groups: (1) a control group, (2) a group fed 25% ethanol, (3) a group fed 25% ethanol and 250 mg/kg BW of fucoidan (25% ethanol+FUCO250), and (4) a group fed 25% ethanol and 500 mg/kg BW of fucoidan (25% ethanol+FUCO500). Each group was fed orally two times per day for 15 days. Liver weights in the 25% ethanol group were increased compared to the control group, while liver weights in the 25% ethanol+FUCO500 group were significantly decreased compared to the 25% ethanol group (p<0.05). Plasma concentrations of triglyceride, cholesterol, and LDL-cholesterol were elevated in the 25% ethanol group; however, these levels in the 25% ethanol+FUCO250 group were significantly decreased compared to the 25% ethanol group (p<0.05). The glutamic-pyruvic transaminase activity of the 25% ethanol+FUCO500 group also was significantly lower than the 25% ethanol group (p<0.05). These results indicate that fucoidan might protect against acute alcohol-induced liver injury.