• Journal of Life Science
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• v.16 no.1
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• pp.95-100
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• 2006

This study was carried out to investigate the effects of Salicornia herbacea L. (SH) on carbon tetrachloride $(CCl_4)-induced$ hepatotoxicity. Sprague-Dawley rats were intraperitoneally administered the SH at 100 mg/kg per day for two weeks. Then single dose of $CCl_4$ (3.3 ml/kg) was injected into rats. Twelve hours later, they were anesthesized with ether and dissected. $SH-CCl_4-administered$ group showed $65.56\%\;and\;59.04\%$ of inhibitory effects in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, compared to $CCl_4-treated$ group (p<0.05). Malonedialdehyde (MDA) levels of $SH-CCl_4-administered$ group in liver homogenate and mitochondria were significantly inhibited by $53.74\%,\;89.86\%$, and respectively, compared to $CCl_4-treated$ group (p<0.05). Superoxide dismutase (SOD) activities of $SH-CCl_4-administered$ group in liver homogenate and mitochondria were significantly inhibited by $42.51\%,\;and\;38.42\%$, respectively, compared to $CCl_4-treated$ group (p<0.05). The histological examinations showed that the liver cell necrosis and centrilobular congestive aggregation induced by $CCl_4$ were clearly eliminated by the administration of SH. These results suggest that SH could have the protective effects against hepatotoxicity.

• Journal of Food Hygiene and Safety
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• v.26 no.3
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• pp.235-241
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• 2011

Although the vegetable Angelica keiskei (AK) has widely been utilized for the purpose of general health improvement among Korean population, its functionalities are not very well defined. In this study, we examined the effects of methanol extract of AK in rats on the biochemical changes induced by two hepatotoxins, D-galactosamine (GalN) and carbon tetrachloride ($CCl_4$). AK was orally administered once daily for 7 days to male rats at 200 and 500 mg/kg, before hepatotoxins. Effects of AK were assessed 24 hr later. AK pretreatments at 200 and 500 mg/kg significantly blunted GalN-induced elevation in liver lipid peroxidation, plasma aspartate-transaminase (AST) and alanine-transaminase (ALT) activities. AK also prevented, after 500 mg/kg but not after 200 mg/kg, the GalN-induced elevation in triglyceride, total cholesterol and LDL-cholesterol levels. Differently from against GalN-induced toxicity, AK did further elevate the $CCl_4$-induced rise in AST, ALT and lipid peroxidation. These results suggest that AK, when pre-administered prior to GalN, exerted protective effects against GalN-induced hepatotoxicity, in contrast however, AK exacerbated that induced by $CCl_4$. To explore possible mechanism for the toxicity-potentiating effects of AK on $CCl_4$, the activity of hepatic drug metabolism after AK treatment was assessed. It was observed that AK increased the activity of aniline hydroxaylase, a cytochrome P450 isoenzyme responsible for metabolic activation of $CCl_4$. This finding suggests that hepatoprotective effects of AK are not equally expected depending on hepatotoxins employed.

• Biomolecules & Therapeutics
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• v.20 no.4
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• pp.406-412
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• 2012

This study was performed to examine the hepatoprotective effect of isorhamnetin-3-O-galactoside, a flavonoid glycoside isolated from Artemisia capillaris Thunberg (Compositae), against carbon tetrachloride ($CCl_4$)-induced hepatic injury. Mice were treated intraperitoneally with vehicle or isorhamnetin-3-O-galactoside (50, 100, and 200 mg/kg) 30 min before and 2 h after $CCl_4$ (20 ${\mu}l/kg$) injection. Serum aminotransferase activities and hepatic level of malondialdehyde were significantly higher after $CCl_4$ treatment, and these increases were attenuated by isorhamnetin-3-O-galactoside. $CCl_4$ markedly increased serum tumor necrosis factor-${\alpha}$ level, which was reduced by isorhamnetin-3-O-galactoside. The levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and heme oxygenase-1 (HO-1) protein and their mRNA expression levels were significantly increased after $CCl_4$ injection. The levels of HO-1 protein and mRNA expression levels were augmented by isorhamnetin-3-O-galactoside, while isorhamnetin-3-O-galactoside attenuated the increases in iNOS and COX-2 protein and mRNA expression levels. $CCl_4$ increased the level of phosphorylated c-Jun N-terminal kinase, extracellular signal-regulated kinase and p38, and isorhamnetin-3-O-galactoside reduced these increases. The nuclear translocation of nuclear factor kappa B (NF-${\kappa}B$), activating protein-1, and nuclear factor erythroid 2-related factor 2 (Nrf2) were significantly increased after $CCl_4$ administration. Isorhamnetin-3-O-galactoside attenuated the increases of NF-${\kappa}B$ and c-Jun nuclear translocation, while it augmented the nuclear level of Nrf2. These results suggest that isorhamnetin-3-O-galactoside ameliorates $CCl_4$-induced hepatic damage by enhancing the anti-oxidative defense system and reducing the inflammatory signaling pathways.

• Korean Journal of Pharmacognosy
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• v.29 no.2
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• pp.146-148
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• 1998

The increased AST and ALT activities of rat serum disturbed by $CCl_4-intoxication$ intoxication were significantly inhibited by silymarin and biphenyl dimethylene dicarboxylate at the oral doses of 150 and 5 mg/kg, respectively. The combined administration of the drugs showed remarkable inhibition of the enzyme activities. This fact may suggest that the two drugs have potentiative action in this experiment.

• Journal of Sericultural and Entomological Science
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• v.50 no.2
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• pp.93-100
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• 2012

To investigate the effects of Protaetia. brevitarsis extracts on the protection against liver damage by carbon tetrachloride($CCl_4$) 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 P.brevitarsis showed significantly low activities of GPT, bile acid, and bilirubin, indicating an excellent protective effect against liver damage by $CCl_4$. Especially, below molecular weight 1,000 blew the water to have 32.1% recovery degree. In the seconde experiment, serum GPT activity was significantly decreased in water fraction of P. brevitarsis compared to $CCl_4$ treatment by 98.2%. Serum concentration of bile acid and bilirubin were tended to increased by $CCl_4$ treatment, but water fraction of P. brevitarsis and silymarin recovered the level. These consistent results in vitro and in vivo suggest that the extracts of P. brevitarsis may have strong protective effects against liver damage induced by the potential toxicants such as $CCl_4$.

• Advances in Traditional Medicine
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• v.9 no.3
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• pp.225-231
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• 2009

The present study deals with the amelioration by Lagerstroemia speciosa Linn. leaf extract against hepatotoxicity induced by carbon tetrachloride ($CCl_4$), which was evaluated in terms of serum marker enzymes like serum glutamate pyruvate transaminase, serum glutamate oxaloacetate transaminase, alkaline phosphatase, serum total bilirubin, total protein levels along with concomitant hepatic and antioxidants like superoxide dismutase, catalase, glutathione, glutathione peroxidase and lipid peroxidation enzymes were monitored. These biochemical parameters altered by the single dose level of $CCl_4$ (0.75 ml/kg body weight, i.p). Pre treatment with L. speciosa prior to the administration of $CCl_4$, at the doses of 50 and 250 mg/kg. body weight/day, p.o. for 7 days, significantly restored all the serum and liver tissue parameters near to the normal levels, respectively. Silymarin was used as a reference standard, prior to the administration of $CCl_4$ to rats. These findings indicate the protective potential of L. speciosa against hepato toxicity which possibly involve mechanism related to its ability of selective inhibitors of (reactive oxygen species like antioxidants brought about significant inhibition of TBARS suggesting possible involvement of $O_2{\cdot}-$, $HO_2{\cdot}$, and ${\cdot}OH$. In conclusion, the amelioration may be attributed to the synergistic effects of its constituents rather than to any single factor as the leaves are rich in tannins, sterols, flavonoids, saponins etc.

• Journal of Pharmacopuncture
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• v.9 no.1
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• pp.45-52
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• 2006

Objectives : This study was aimed at investigating liver protection mechanism of Moschus by inducing liver toxicity through $CCl_4$ in mice and evaluated histological and serological findings. Methods : Experiment groups was categorized into untreated normal group, $CCl_4$ treated control group, and orally administered Moschus experiment group. At the termination of experiment, gross examination of the liver as well as histological findings, and Total protein, Total bilirubin, Direct bilirubin SGOT, SGPT, and ALP contents in the serum were evaluated. Results : 1. For gross examination and histological findings, $CCl_4$ treated control group showed destroyed lobular structure, increased fibrosis, as well as hepatic cirrhosis. For the group treated with Moschus, the lobular structure suffered less damage, and showed lower level of fibrosis and liver cirrhosis compared to the control group. 2. For serum analysis, Total protein were significantly increased in the Moschus experiment group than the control group. 3. Total bilirubin didn't show significant differences between the two groups. but direct bilirubin was significantly increased in the Moschus experiment group than the control group. 4. SGOT, SGPT, were significantly decreased in the normal and Moschus experiment groups compared to the control group. 5. ALP was significantly decreased in the normal group compared to the control group, but Moschus experiment group didn't show significant differences compared to the control group. Conclusion : Taken together, Moschus can be effectively used for recovering the liver functions and further researches must be conducted to verify the efficacies of Moschus bile juice.

• Journal of Food Hygiene and Safety
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• v.19 no.3
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• pp.105-111
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• 2004

Green tea catechin (GTC) is known to have a wide variety of pharmacological activites. In the present study, the effects of GTC on acute hepatotoxicity induced by carbon tetrachloride ($CCl_4$) and galactosamine were examined in rats. Two doses (50 or 100 mg/kg) of GTC were administered to rats orally for 3 days befor or after the induction of hepatotoxicity. A hepatotoxicity was induced by the inpraperitoneal injection of the $CCl_4$ (0.5 ml/kg) or galactosamine (400 mg/kg). GTC(50 mg/kg) reduced the aspartate aminotransferase (AST) and alanine aminotransferase (ALT) level of the $CCl_4$-intoxicated rats in the pre-treatment group (from 262${\pm}$11, 80${\pm}$19 to 153${\pm}$22, 55${\pm}$25), and also in the post-treatment group (from 156${\pm}$40, 105${\pm}$3 to 106${\pm}$22, 55${\pm}$9), respectively. And GTC (50 mg/kg) also reduced the levels of AST and ALT in both pre-treatment (from 576${\pm}$24, 276${\pm}$68 to 236${\pm}$13, 115${\pm}$13) and post-treatment (from 233${\pm}$54, 137${\pm}$11 to 119${\pm}$23, 44${\pm}$17) when induced by galactosamine. GTC also showed the inhibition of pathogenesis of hepatocyte of $CCl_{4^-}$ and galatosamine-intoxicated rat. These results suggest that green tea catechin (GTC) may be useful fur the prevention and therapy of hepatotoxic pathogenesis.

• Toxicological Research
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• v.28 no.3
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• pp.165-172
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• 2012

Raphanus sativus (Cruciferaceae), commonly known as radish is widely available throughout the world. From antiquity it has been used in folk medicine as a natural drug against many toxicants. The present study was designed to evaluate the hepatoprotective activity of radish (Raphanus sativus) enzyme extract (REE) in vitro and in vivo test. The $IC_{50}$ values of REE in human liver derived HepG2 cells was over 5,000 ${\mu}g/ml$ in tested maximum concentration. The effect of REE to protect tacrine-induced cytotoxicity in HepG2 cells was evaluated by MTT assay. REE showed their hepatoprotective activities on tacrine-induced cytotoxicity and the $EC_{50}$ value was 1,250 ${\mu}g/ml$. Silymarin, an antihepatotoxic agent used as a positive control exhibited 59.7% hepatoprotective activity at 100 ${\mu}g/ml$. Moreover, we tested the effect of REE on carbon tetrachloride ($CCl_4$)-induced liver toxicity in rats. REE at dose of 50 and 100 mg/kg and silymarin at dose of 50 mg/kg were orally administered to $CCl_4$-treated rats. The results showed that REE and silymarin significantly reduced the elevated levels of serum enzyme markers induced by $CCl_4$. The biochemical data were supported by evaluation with liver histopathology. These findings suggest that REE, can significantly diminish hepatic damage by toxic agent such as tacrine or $CCl_4$.

• Journal of Life Science
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• v.20 no.5
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• pp.782-788
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• 2010

The protective effects of a powder mixed with solid-cultured and liquid-cultured Lentinus edodes mycelia (2 : 1, w/w) (designate LED) with different doses of carbon tetrachloride ($CCl_4$) on induced hepatotoxicity in male Sprague-Dawley (SD) rats was investigated. The rats were divided into seven groups (6 rats/group) and the following substances were administered orally to each group: Vehicle (0.2 ml distilled water), Control (0.2 ml distilled water), LED (LED 100, 200, 300 and 400 mg/kg BW in 0.2 ml distilled water), and Silymarin (200 mg/Kg BW in 0.2 ml distilled water). After two weeks of daily administration, all groups except for the Vehiclegroup were subjected to abdominal injection with $CCl_4$ ($CCl_4$ : corn oil, 1 : 1 v/v; 0.5 ml/kg BW). One day later, blood and liver samples were collected to analyze biomarkers. All LED treatments elevated hepatic superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH peroxidase) activities, and reduced thiobarbituric reactive substances (TBARS), tumor necrosis factor-$\alpha$ (TNF-$\alpha$), interleukin-$1{\beta}$ (IL-$1{\beta}$) and interleukin-6 (IL-6), resulting in the reduction of glutamate-oxalate transaminase (GOT), glutamate-pyruvate transaminase (GPT) and lactic acid dehydrogenase (LDH) activities in plasma. These results indicate that LED effectively protected SD rat hepatotoxicity induced by $CCl_4$ through its antioxidative activity and reduction of some cytokines. The highest efficacy was found in LED 200 mg/kg BW, showing potential as a useful material for protection from hepatotoxicity in humans.