• Food Science and Biotechnology
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• v.16 no.6
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• pp.967-974
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• 2007

The present work is aimed to evaluate the protective effect of glutathione-enriched Saccharomyces cerevisiae FF-8 strain on carbon tetrachloride ($CCl_4$)-induced hepatotoxicity and oxidative stress in rats. The activities of liver markers (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase), lipid peroxidative index (thiobarbituric acid-reactive substances), and the antioxidant status (reduced glutathione) were used to monitor those protective roles of FF-8 strain. The liver marker enzymes in plasma and the lipid peroxidation in the liver were increased when $CCl_4$ was treated but these were significantly decreased by FF-8 strain treatment. The hepatic concentration of glutathione in the current glutathione-enriched FF-8 strain fed animal was approximately twice as high as the normal, but this was slightly increased in response to $CCl_4$ plus glutathione-enriched FF-8 strain. The increased liver triglyceride concentration due to the $CCl_4$ treatment was significantly decreased by FF-8 strain and the reduced level reached to that of normal group. Administration of FF-8 strain in normal rat did not show any signs of harmful effects. Therefore, the current findings suggest that FF-8 strain could be an effective antioxidant with no or negligible side-effects and it might be useful for the purpose of protection treatment of hepatotoxicity and oxidative stress in $CCl_4$-treatment in rat.

• YAKHAK HOEJI
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• v.43 no.6
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• pp.827-833
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• 1999

In this study, we have investigated the effect of Biphenyl Dimethyl Dicarboxylate (DDB), a synthetic analogue of Schizandrin C isolated from Schizandrae Fructus on cytochrome $P_450$ lAl and 2Bl, and the protective mechanism against $CCl_4-induced$ hepatotoxicity in rat liver. After DDB was administered into male rats for different periods of time (1~7 days) and with different doses (25, 50, 100 and 200 mg/kg), mRNA levels of CYPlAl were measured by polymearse chain reaction (PCR) and assayed the activities of CYPlAl specific ethoxyresorufin-O-dealkylase (EROD) and CYP2Bl specific benzyloxyresorufin-O-dealkylase (BROD). DDB treatment resulted in increase in CYP2Bl mRNA level and BROD activity, whereas there was no change in CYPlAl mRNA level and EROD activity. This effect of DDB was time-and dose-dependent and reached maximal level by 3 day and 200 mg/kg treatment. In addition, rats were pre-treated with DDB at doses of 25, 50 or 100 mg/kg daily for 4 days, 3-hr after final treatment on the 4th day, $CCl_4$ 0.3ml/kg was intraperitonially injected into the rats to examine the effect of DDB on $CCl_4-induced$ hepatic injury. Serum levels of ALT and AST were determined and histopathological examination was done in rat liver. Furthermore, we have measured hepatic microsomal malondialdehyde(MDA) level, a parameter of lipid peroxidation. Based on serum ALT level and lipid peroxidation, pretreatment of DDB, 50 mg/kg appeared the most protective effect against $CCl_4-induced$ heapatotoxity. These results indicate that DDB stimulates CYP2Bl mRNA level and BROD activity in time and dose dependent manner and suggest that protective effect of DDB on $CCl_4-induced$ hepatotoxicity may be mediated through free radical scavenging.

• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.30.2-30.2
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• 2008

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.124.2-124.2
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• 2007

See Full Text

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.125.1-125.1
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• 2007

See Full Text

• Journal of Life Science
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• v.20 no.1
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• pp.133-141
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• 2010

The protective effect of a mixed powder from solid-cultured and liquid-cultured Lentinus edodes mycelia (2:1, w/w) (designate LED) on the carbon tetrachloride ($CCl_4$)- and ethanol-induced hepatotoxicity of male Sprague-Dawley (SD) rat was investigated. In the $CCl_4$-induced rat hepatotoxicity experiment, rats of 4 groups (6 rats/group) were administere with Normal (0.2 ml distilled water), Control (0.2 ml distilled water), LED (LED 200 mg/kg BW + 0.2 ml distilled water), and Silymarin (200 mg/kg BW + 0.2 ml distilled water), p.o., daily for 2 weeks. Afterwards, all groups except for the Normal group were subjected to abdominal injection with $CCl_4$ ($CCl_4$ : corn oil, 1:1 v/v; 0.5 ml/kg BW). For the ethanol- induced rat hepatotoxicity experiment, rats were divided into 5 groups (5 rats/group): Normal; Pair-fed control (PFC); Control (ethanol); LED (ethanol + LED 200 mg/kg BW); and Silymarin (ethanol + silymarin 200 mg/kg BW). Rats of the Normal and PFC groups were fed a basal liquid diet, and rats of the Control, LED, and Silymarin groups were fed a liquid ethanol diet containing LED or Silymarin. Eight weeks later, blood and liver samples were collected to analyze biomarkers. In $CCl_4$-induced SD rats, LED elevated hepatic superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH peroxidase) activities and thiobarbituric reactive substances (TBARS) were reduced, resulting in the reduction of glutamate-oxalate transaminase (GOT), glutamate-pyruvate transaminase (GPT) and lactic dehydrogenase (LDH) activities in plasma. Similar results of these enzymes and biochemical markers in both liver tissues and plasma were seen in ethanol-induced hepatotoxicity of SD rats. In addition, elevated alcohol dehydrogenase (ADH) activity and reduced expression of cytochrome p450 mixed monooxygenase enzyme (CYP2E1) were seen in liver tissues from ethanol-treated rats by LED treatment. These effects of LED were similar to those of Silymarin. In in vitro experiments, LED showed antioxidant activity in a 2,2-diphenyl-1-picrylhydrazyl (DPPH) system and mouse liver mitochondria system induced by NADPH/$Fe^{2+}$ and cumine hydroperoxide (CuOOH). These results indicate that LED protected SD rat hepatotoxicity, induced by $CCl_4$ and ethanol, through its antioxidative activity and might be useful as a material for protection from hepatoxicity in humans.

• The Journal of Pediatrics of Korean Medicine
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• v.30 no.3
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• pp.69-77
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• 2016

Objectives This study is to investigate whether oral administration of Farfarae flos, JCT (Jeong-cheon-tang), CPT (Cheong-pye-tang) and CPK (Cheong-pye-tang- ga-kwandonghwa) will affect both the levels of serum GOT, GPT, blood urea nitrogen (BUN) and creatinine in SD rats or not, and will change body weight of the rats. Materials and Methods 18 SD rats were randomly divided into 6 groups - including a control group (vehicle 2 ml/rat), Farfarae flos water extract (extract 2 ml/rat), Farfarae flos fine powder (emulsion 2 ml/rat), JCT (extract 2 ml/rat), CPT (extract 2 ml/rat) and CPK (extract 2 ml/rat) group. The drugs were administered to rats for 2 weeks or 30 days (for control and Farfarae flos fine powder group only) and serum GOT/GPT activities and BUN/creatinine concentrations were measured. Also, the changes of body weights of each rat was measured. Results (1) Farfarae flos water extract, Farfarae flos fine powder emulsion, JCT and CPT and CPK did not cause any changes in serum GOT/GPT activities and BUN/creatinine concentrations compared to the ones in control group. (2) There are no significant changes in rats' body weight among the experimental groups during the experimental period. Conclusions Contrary to the reports on human data, 2 weeks or 30 days of oral administrations of Farfarae flos itself and decoctions containing Farfarae flos did not provoke hepatotoxicity and nephrotoxicity.

• Korean Journal of Veterinary Research
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• v.51 no.2
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• pp.159-164
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• 2011

Alcohol abuse and its medical and social consequences are a major health problem in many areas of the world. Korean red ginseng (KRG) has been traditionally used for the treatment of liver disease. This study was conducted to evaluate the hepatoprotective effects of KRG against hepatotoxicity in Sprague- Dawley rats treated with ethanol (EtOH). Administration of EtOH for 20 days induced significant changes in serum biochemical parameters (aspartate aminotransferase, alanine transaminase, and glucose) accompanied by histological changes in the liver tissue. Treatment with KRG prior to administration of EtOH inhibited the EtOH-induced biochemical and histological changes of the liver. In perfused rat livers, administration of EtOH caused an increase in lactate dehydrogenase (LDH) release into the perfusate and activated the pro-apoptotic Bax protein but inhibited the anti-apoptotic Bcl-2 protein. Pretreatment with KRG prior to administration of EtOH decreased the EtOH-induced LDH release and inhibition of Bcl-2 protein. These results suggest that KRG exerts anti-apoptotic effects and alleviated EtOH-induced liver injury in rats.

• Preventive Nutrition and Food Science
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• v.9 no.3
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• pp.245-252
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• 2004

This study investigated the effects of an ethanol extract of Allium monanthum MAX. (AME) on ethanol-induced hepatotoxicity in rat liver. Sprague-Dawley rats weighing 100～150 g, were divided into 5 groups; normal group (NOR), AME 200 mg/kg treated group (S1), ethanol (35%, 10 mL/kg) treated group (S2), AME 200 mg/kg and ethanol (35%, 10 mL/kg) treated group (S3) and AME 400 mg/kg and alcohol (35%, 10 mL/kg) treated group (S4). AME was fractionated by the following solvents: n-hexane, chloroform, EtOAC and n-BuOH. Antioxidant index of the n-BuOH fraction was 600 ppm, highest among fractions. The growth rate and feed efficiency ratio were decreased by ethanol, but gradually increased to the corresponding level of the normal group by administering AME. The serum ALT activities that were elevated by ethanol were significantly decreased by AME administration. It was also observed that the hepatic activities of SOD, catalase, xanthine oxidase and GSH-Px that were increased by ethanol were also markedly decreased in the AME treated group with compared to ETB. These results suggest that ethanol extracts of Allium monanthum MAX. may have a protective effect on ethanol-induced hepatotoxicity in rat liver.

• Journal of Preventive Medicine and Public Health
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• v.33 no.1
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• pp.117-124
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• 2000

Objectives : It is the objective of this study to compare hepatotoxicity of nickel chloride and cadmium chloride with each other through IPRL(Isolated Perfused Rat Liver) method. Methods : Biochemical indicator of hepatic function such as AST(aspartate aminotransferase), ALT(alanine aminotransferase), LDH(lactate dehydrogenase) and perfusion flow rate were used as the indicator of hepatotoxicity. Oxygen consumption rate were used as vability indicator. $300({\pm}50)g$ - weighted rats were allocated randomly to each group($0{\mu}M,\;50{\mu}M,\;200{\mu}M\;NiCl_2\;and\;CdCl_2$ exposure) by 5, totally 25. After Krebs-Ringer bicarbonate butler solution flowed into the penal vein and passed the liver cell, it flowed out of vena cava. Liver was administered with each $NiCl_2\;and\;CdCl_2$ of each concentration and observed with buffer solution sampling time. Butler which got out of liver was sampled and then biochemical indicator of hepatotoxicity was measured. Results : AST, ALT, and LDH in buffer increased with sampling time much more in $CdCl_2$ exposure group than $NiCl_2$ exposure group in both 50 and $200{\mu}M$ and statistical significance w3s verified with 2-way repeated ANOVA. Viability was decreased more and more in all substances during passed time. Conclusions : It is inferred that $CdCl_2$ has stronger hepatotoxicity than $NiCl_2$. IPRL method would be used widely for acute hepatotoxicity when considerating the benefit of it.