• Journal of Haehwa Medicine
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• v.9 no.2
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• pp.111-121
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• 2001

In order to evaluate the protective effect of Kamicheungkantang(KCKT) on hepatic damage induced by $CCl_4$, the study was done. The blood chemistry and histological study were done following oral administration with materials. The results were obtained as follows. 1. KCKT extracts didn't show cytotoxicity against BALB/C mouse lung fibroblast cell. 2. In the hepatotoxicity with $CCl_4$, serum alanine aminotransferase(ALT) was significantly decreased in KCKT treated group as compared with control group. 3. In the hepatotoxicity with $CCl_4$, serum aspartate aminotransferase (AST) was significantly decreased in KCKT treated group as compared with control group. 4. In the hepatotoxicity with $CCl_4$, serum alkaline phosphatase(ALP) was significantly decreased in KCKT treated group as compared with control group. 5. In the hepatotoxicity with $CCl_4$, serum lactate dehydrogenase(LDH> was insignificantly decreased in KCKT but insignificantly as compared with control group. 6. In the hepatotoxicity with $CCl_4$, serum cholestorol was significantly decreased in KCKT treated group as compared with control group. 7. In the hepatotoxicity with $CCl_4$, serum triglyceride was insignificantly decreased in KCKT treated groups as compared with data of control. 8. In the hepatotoxicity with $CCl_4$, serum total bilirubin, direct bilirubin, ${\gamma}$-GTP were not changed in KCKT treated groups as compared with data of control. 9. In histopathological changes, fatty changes, vacuole, nucleotic changes and fibrosis were observed in control group and degree of changes was increased over time. Whereas no differences were observed in KCKT treated group These results suggested that KCKT extracts might be usefully applied for treatment of hapatic disease and also it was necessary to do more studies about its mechanisms.

• Journal of Food Hygiene and Safety
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• v.14 no.2
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• pp.172-178
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• 1999

Previous studies have shown that methanol extract and its butanol fraction of Carthamus tinctorius L. Semen have the hepatoprotective effect on the CCl4-induced hepatotoxicity. The hepatoprotective effect of subfractions has been evaluated by analyzing blood and hepatocyte biochemical analyses and biotransformation enzyme analyses. Treatment of BS-5, subfraction has significantly decreased the activities of alanine aminotransferase and aspartate aminotransferase. In addition, the levels of cholesterol and triglyceride in liver have been decreased as compared with that of CCl4 treated rats. The hepatoprotective effect of BS-5, subfraction on the CCl4-induced hepatotoxicity would be mediated of the attenuation of the level of cytochrome P450 and the enhancement of the activity of glutathion S-transferase.

• 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.

• 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.

• Biomolecules & Therapeutics
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• v.8 no.4
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• pp.293-298
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• 2000

Bergenin is a C-glucoside of 4-O-methyl gallic acid that has been isolated from the cortex of Mallotus japonicus (Euphorbiaceae). Acetylbergenin was synthesized by acetylation from bergenin to increase lipophilic and physiological activities. The therapeutic effects of bergenin and acetylbergenin were evaluated against carbon tetrachloride ($CCl_4$)-induced hepatotoxicity in rats. Bergenin and acetylbergenin were administered orally once daily for successive 5 days, after the intraperitoneal injection of a mixture 0.5 m1/kg of $CCl_4$ in olive oil (1:1). The substantially elevated serum enzymatic activities of alanine/aspartate aminotransferase, sorbitol dehydrogenase and ${\gamma}$-glutamyltransferase induced by $CCl_4$ were restored towards normalization by posttreatment with bergenin and acetylbergenin. Bergenin and acetylbergenin also significantly prevented the elevation of hepatic malondialdehyde formation and depletion of glutathione content induced by $CCl_4$ in a dose dependent fashion. In addition, the decreased activities of glutathione S-transferase and glutathione reductase were restored towards normalization. These results suggest that therapeutic effects of bergenin and acetylbergenin may be related complex mechanisms that involve prevention of lipid peroxidation and preservation of hepatic GSH. The results of this study clearly indicate that bergenin and acetylbergenin have potent hepatothrapeutic action against $CCl_4$-induced hepatotoxicity in rats. In addition, acetylbergenin 50 mgHg showed almost the same levels of hepatoprotective activity as those of bergenin 100 mgAg, indicating the fact that lipophilic acetylbergenin is more effective in the hepatoprotective action against $CCl_4$ than bergenin.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.1
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• pp.102-106
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• 2001

To investigate the effects of leek green juice on the damaged liver of $CCl_{4}$-treated rats, Sprague-Dawley male rats weighing about 100g, were divided into 4 groups ; control group (CON), leek green juice-administered group (LGJ), $CCl_{4}$-treated group (CCL) and leek green juice and $CCl_{4}$-treated group (LCL). After 6 weeks, the activities of sGPT and sGOT, and content of hepatic TBA-reactants, elevated by $CCl_{4}$ treatment, were markedly decreased by administering leek green juice, compared to CCL. It was also observed that activities of hepatic SOD and GSH-Px were elevated by $CCl_{4}$-treatment as compared to CON, but concomitant treatment of leek green juice and $CCl_{4}$ decreased those levels adjacent to CON, whereas catalase activity did not show significant decreasing effects compared to CCL. The hepatic content of glutathione, decreased by $CCl_{4}$, was more abundantly increased by leek green juice administration than by CCL. These results suggest that leek green juice is believed to b a possible protective effect for the carbon tetrachloride-induced hepatotoxicity in rat liver.

• YAKHAK HOEJI
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• v.40 no.3
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• pp.320-325
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• 1996

In order to evaluate the protective effects of galangin on $CCl_4$-induced hepatotoxicity, GOT, GPT and malondialdehyde(MDA) values were measured in ICR mice. Galangin,a flavonoid compound, was administered orally for six days and immediately $CCl_4$ was injected intraperitoneally after the last dose of galangin. Mice were sacrificed at 24h after the administration of $CCl_4$. In the multiple pre-treatments for 6 consecutive days, galangin showed more potent protective effects than silymarin as reference active compound in serum GOT, GPT and MDA values in the liver at all doses tested. Antioxidative activity was determined by measuring the amounts of MDA formed from ethyl linoleate by $H_2O_2$ in vitro. Galangin showed higher inhibition than silymarin. These results demonstrate a possible hepato-protective role of galangin against $CCl_4$-induced hepatotoxicity in vivo and $H_2O_2$-induced lipid peroxidation in vitro. Therefore, galangin may be capable of protecting hepatotoxicity.

• Toxicological Research
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• v.8 no.2
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• pp.265-272
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• 1992

Effects of repeated physical exercise on the carbon tetrachloride ($CCl_4$) hepatotoxicity were examined in adult female rats. Rats were introduced into a cylindrical rotating cage and forced to exercise for 1 hr each day, 6days/week, for 5 consecutive weeks at a speed starting from 10m/min, increased by 1m/min per day until the speed reached 27m/min. Significantly less body weight gain was observed in the exercise group suggesting that physical fitness had been induced in these animals. Eighteen hours following termination of the last exercise bout rats were treated with $CCl_4$(2 mmol/kg.ip). The $CCl_4$-induced heptotoxicity was significantly potentiated in the repeated exercise group compared to the resting sedentary animals as determined by changes in serum sorbitol dehydrogenase (SDH), glutamic oxaloacetic transaminase(GOT), glutamic pyruvic transaminase (GPT), and glucose-6-phosphatase(G-6-Pase) activities when measured 24hrs following the $CCl_4$ treatment. Hepatic drug metabolizing activity was determined in order to elucidate the underlying mechanism of potentiating action of the $CCl_4$ hepatotoxicity induced by repeated physical exercise. Repeated exercise increased the hepatic microsomal cytochrome P-450 contents and aminopyrine N-demethylase activity. The results suggest that the potentiation of $CCl_4$ hepatotoxicity by repeated exercise is associated with induction of the mixed function oxidase (MFO) enzyme system mediating the metabolism of $CCl_4$ to its active metabolite(s).

• Herbal Formula Science
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• v.8 no.1
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• pp.129-146
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• 2000

This study was carried out to investigate the effects of Solanum lyratum Extract (SLE) on the recovery of liver in $CCI_{4}-intoxicated$ mice. In this study, ICR-Mice were divided into 3 experimental groups; Normal group was fed basal diet and was fed bassal diet for 2 Weeks, sample group was injected $CCl_{4}\;(0.6m{\ell}/kg)$ and was fed basal diet for 2 weeks, sample group was injected $CCl_{4}\;(0.6m{\ell}/kg)$ and was fed the SLE 500mg/kg fod 2 Weeks. In sample group, the level of serum AST, ALT, ALP activity decreased significantly compared with control group. This results suggest that SLE has appreciable therapeutic effect on $CCI_4$ induced hepatotoxicity. In sample group, the level of LPO in liver homogenates decreased significantly compared with control group. In sample group. the level of GSH, catalase in liver homogenates increased significantly compared with control group. This results suggest that SLE has appreciable antioxidant effect on $CCI_4induced hepatotoxicity. In conclusion the results suggest that SLE has appreciable therapeutic effect and antioxidant effect on $CCI_4$ induced hepatotoxicity.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.47 no.3
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• pp.204-210
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• 2014

The brown alga Saccharina japonica is consumed as a foodstuff in many countries. Carbon tetrachloride ($CCl_4$) is a potent hepatotoxin that is used to assess hepatotoxicity in animal models. This study assessed the protective effect of S. japonica extract (SJE) on $CCl_4$-induced acute liver injury in rats. Experimental rats were divided into the following three groups: control, $CCl_4$, and $CCl_4$+SJE; the latter two groups were given 150 or 300 mg SJE/kg orally for 10 days. Three hours after the final treatment, all rats-except for those in the control group-were administered intraperitoneal injections of $CCl_4$. One day later, blood and liver samples were collected for evaluation biomarker of levels. Aspartate transaminase (APT; GPT) and alanine aminotransferase (ALT; GOT) levels were markedly lower in the $CCl_4$+SJE group than the $CCl_4$ group. The hepatic superoxide dismutase (SOD) activity of the $CCl_4$+SJE group was significantly lower than that of the $CCl_4$ group. In comparison, glutathione S-transferase (GSH) and catalase (CAT) levels were significantly higher in the $CCl_4$+SJE group. Western blotting revealed that SJE attenuated the $CCl_4$-induced EGFR and MAPK activity in the liver. Thus, we conclude that SJE protects against $CCl_4$-induced hepatotoxicity.