• Natural Product Sciences
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• v.14 no.2
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• pp.95-99
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• 2008

In a project to study the hepatroprotective effect of some plant extracts four plants Ephedra foliate Boiss, Alhagi maurorum Medikus, Capsella bursa-pastoris (L.) Medik. and Hibiscus sabdariffa L. were studied. The ethanol extract of the aerial part of the first three plants and the flowers of H. sabdariffa were subjected to hepatoprotective assays using Wistar albino rats. Liver injury induced in rats using carbon tetrachloride. The biochemical parameters; serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP) and total bilirubin were estimated as reflection of the liver condition. Based on the good results of the biochemical parameters measurements, histopathological study was performed on the liver of rats treated with E. foliate. The normal appearance of hepatocytes indicated a good protection of the extract from carbon tetrachloride hepatotoxicity. All the results were compared with silymarin, the reference hepatoprotective drug.

• YAKHAK HOEJI
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• v.41 no.5
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• pp.622-628
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• 1997

Hepatic cirrhosis is a common response to chronic liver injury from many causes and is one of the most common cause of all deaths. This study was carried out to compare experimental hepatic cirrhosis in rats to understand this disease and to apply for the pharmacokinetics in disease state. Following three kinds of experimental models were induced; 1) Bile duct ligation/scission (BDL/S), 2) N, N-dimethylnitrosamine(DMN), 3) Carbon tetrachloride. The hepatic cirrhosis was characterized by examing the liver/body weight ratio, serum biochemical values, hydroxyproline content in liver and histopathological lesions in cirrhotic rat liver. The results are as follows : (1) In BDL/S, the liver was enlarged to 250% of normal liver. In contrast the liver was shrinked to 48% and 78% of the normal liver in DMN and carbon tetrachloride, respectively. (2) In carbon tetrachloride and BDL/S, the serum ALT, AST, ALP and total bilirubin levels were significantly increased to 200~300% of normal level, while ALT and total bilirubin levels were significantly increased in DMN group. (3) Hydroxyproline content in cirrhotic rat liver was significantly 200~500% higher than that of normal liver. (4) Nodular formation with fibrosis was observed in BDL/S, DMN, carbon tetrachloride induced cirrhotic rat liver.

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.2
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• pp.326-332
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• 1998

The effect of mushroom extracts from Pleurotus ostreatus and Lentinus edodes on carbon tetrachloride(CCl4)-induced hepatotoxicity was investigated. Rats were administered orally each mushroom extract at the dose of 150mg/kg, foolwed by treatment with CCl4. Liver damage was produced in male Sprague-Dawley rats, after 21hrs from dosing with CCl4(0.25ml/kg) which were given intraperitoneally. Liver damage without renal injury was confirmed by measuring plasma enzyme, creatinine and blood analysis and liver analysis. Plasma aminotransferase activity, and levels of cholesterol and triglyceride were analyzed. Plasma alanine aminotransferase and aspartate aminotransferase activities were decreased by 34% and 61.5% in pretreatment group of Lentinus edodes compared with CCl4 treated group, respectively. The adminstration of all mushroom extracts led the plasma cholesterol and triglyceride levels decrease more than the CCl4-treated rats. These results suggest that Lentinus edodes extract protect liver from damage induced by CCl4.

• Food Science and Biotechnology
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• v.14 no.2
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• pp.290-296
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• 2005

Effects of water extract obtained from Chrysanthemum boreale M. (CE) on serum enzyme activities and Kupffer cells of carbon tetrachloride ($CCl_4$)-induced rats were investigated. Thirty-two healthy male Sprague-Dawley rats were divided into normal (N), $CCl_4$-induced (T), CE-supplemented (C), and $CCl_4$-induced and CE-supplemented (TC) groups. $CCl_4$ injection significantly increased aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and alkaline phosphatase activities in serum. Significant increases in total cholesterol and triglyceride concentrations were also observed in $CCl_4$-induced rats. Oral administration of CE at 300 mg/kg body weight significantly decreased serum enzyme levels and suppressed $CCl_4$ hepatotoxicity-induced lipid profile changes. Histological findings showed fatty change, fibrosis and increased number of Kupffer cells in T group. Electron microscopic examination showed increased lysosome content and dilation of rough endoplasmic reticulum within Kupffer cells in T group, whereas CE supplement attenuated liver injury in $CCl_4$-induced liver. These results indicated CE could significantly alleviate CC4-induced hepatotoxicity injury.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.218-223
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• 2018

The liver is an essential organ for the detoxification of exogenous xenobiotics, drugs and toxic substances. The incidence rate of non-alcoholic liver injury increases due to dietary habit change and drug use increase. Our previous study demonstrated that Ecklonia stolonifera (ES) formulation has hepatoprotective effect against alcohol-induced liver injury in rat and tacrine-induced hepatotoxicity in HepG2 cells. This present study was designated to elucidate hepatoprotective effects of ES formulation against carbon tetrachloride ($CCl_4$)-induced liver injury in Sprague Dawley rat. Sixty rats were randomly divided into six groups. The rats were treated orally with ES formulation and silymarin (served as positive control, only 100 mg/kg/day) at a dose of 50, 100, or 200 mg/kg/day for 21 days. Seven days after treatment, liver injury was induced by intraperitoneal injection of $CCl_4$ (1.5 ml/kg, twice a week for 14 days). The administration of $CCl_4$ exhibited significant elevation of hepatic enzymes (like AST and ALT), and decrease of antioxidant related enzymes (superoxide dismutase, glutathione peroxidase and catalase) and glutathione. Then, it leaded to DNA damages (8-oxo-2'-deoxyguanosine) and lipid peroxidation (malondialdehyde). Administration of ES formulation inhibited imbalance of above factors compared to $CCl_4$ induced rat in a dose dependent manner. Real time PCR analysis indicates that CYP2E1 was upregulated in $CCl_4$ induced rat. However, increased gene expression was compromised by ES formulation treatment. These findings suggests that ES formulation could protect hepatotoxicity caused by $CCl_4$ via two pathways: elevation of antioxidant enzymes and normalization of CYP2E1 enzyme.

• Toxicological Research
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• v.30 no.1
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• pp.49-54
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• 2014

In this study, we investigated the hepatoprotective effects of aged black garlic (ABG) in rodent models of liver injury. ABG inhibited carbon tetrachloride-induced elevation of aspartate transaminase (AST) and alanine transaminase (ALT), which are markers of hepatocellular damage, in SD rats. D-galactosamine-induced hepatocellular damage was also suppressed by ABG treatment. However, ABG does not affect the elevation of alkaline phosphatase (ALP), a marker of hepatobilliary damage, in rats treated with carbon tetrachloride or D-galactosamine. We also examined the effect of ABG on high-fat diet (HFD)-induced fatty liver and subsequent liver damage. ABG had no significant effect on body weight increase and plasma lipid profile in HFD-fed mice. However, HFD-induced increase in AST and ALT, but not ALP, was significantly suppressed by ABG treatment. These results demonstrate that ABG has hepatoprotective effects and suggest that ABG supplementation might be a good adjuvant therapy for the management of liver injury.

• Korean Journal of Veterinary Research
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• v.50 no.2
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• pp.145-149
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• 2010

This study was carried out to find whether phenidone (1-phenyl-3-pyrazolidinone), a cyclooxygenase as well as a lipoxygenase inhibitor, exhibits the preventive effect on carbon tetrachloride $(CCl_{4})-induced$ acute liver injury in rats. Rats were pretreated with phenidone at a dose of 50 or 200 mg/kg (p.o.) once daily for 3 consecutive days before $CCl_{4}$ administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Malondialdehyde (MDA) production was determined as an index of lipid peroxidation in the liver and serum. The histopathological changes in the liver were also examined in each group. The reduction in body weights was significantly inhibited in the phenidone-treated group than in the $CCl_{4}$ control group. Significant increase in the relative liver weights of the phenidone-treated groups was observed compared with either the vehicle or $CCl_{4}$ groups. Elevation of serum AST and ALT activities occurred after $CCl_{4}$ treatment was significantly attenuated by the pretreatment with phenidone. The elevation of MDA levels in liver and serum were completely inhibited in phenidone-treated groups. The protective effects on phenidone-treated groups were confirmed histopathologically. These results suggest that phenidone may be a useful protector through modulation of hepatic inflammation in $(CCl_{4})-induced$ acute liver injury.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.208.2-208.2
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• 2002

• Toxicological Research
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• v.25 no.1
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• pp.29-33
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• 2009

Phellinus gilvus (PG) is a widely used mushroom for health promotion. We studied the hepatoprotective effect of the polysaccharide aqueous extract of PG (PGP) against carbon tetrachloride ($CCl_4$)-induced liver injury in rats. Sprague Dawley rats were divided into 5 groups: Normal control, $CCl_4$ control, PGP 50, 100, and 200 mg/kg + $CCl_4$. The levels of serum biochemical parameters, liver lipid peroxide and antioxidant enzymes, and histological appearances were evaluated. The $CCl_4$-induced increments of alanine aminotransferase, asparate aminotransferase, and alkaline phosphatase levels in serum were significantly decreased by PGP-pretreatments. The PGP dose-dependently decreased hepatic malondialdehyde formations in $CCl_4$-treatment groups. Hepatic antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) were elevated by PGP in $CCl_4$-treatment groups. Histopathological evaluation of liver showed that the loss of hepatocytes, fatty changes, swelling and extensive necrosis of hepatocytes in centrilobular regions of the $CCl_4$-treated rats were ameliorated by PGP pretreatment. The PGP has hepatoprotective and antioxidative effects in $CCl_4$-induced liver injury of rat.

• Advances in Traditional Medicine
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• v.4 no.1
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• pp.28-36
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• 2004

The purpose of this study was to investigate the pharmacological effects of low-esterified pectin on carbon tetrachloride $(CCL_4)-induced$ hepatotoxicity in rats. The study included two experiments. In the first experiment the animals were given daily $CCL_4$ through gavage for 7 days and then 10, 50, or 250 mg/kg b.w. of pectin for 21 days. At the end of experiment rats were killed within 24 hours. The increased bilirubin level, enhanced alanine aminotransferase and aspartate aminotransferase activity in plasma induced by $CCL_4$ were partly normalized by pectin administration in a dose-dependent manner. The pectin treatment also resulted in significant recovery of $CCL_4-induced$ decrease of the liver glycogen content. In addition, pectin significantly improved $CCL_4-induced$ alterations of pro-oxidant and antioxidant biochemical parameters in liver and plasma compared to those of rats administered $CCL_4$. In the second experiment the animals were given daily 10, 50 or 250 mg/ kg b.w. of pectin for 21 days before a 7-day administration of $CCL_4$. Rats were killed 24 hours after the end of experiment. Pretreatment with pectin before $CCL_4$ administration resulted in significantly inhibited increase of the blood enzymatic activities of alanine and aspartate aminotransferases and bilirubin level in a dose-dependent manner. Also, preliminary administration of pectin prevented elevation of malondialdehyde and conjugated diene levels in liver and plasma as well as a reduction of glutathione content in liver of rats given $CCL_4$. These results suggest that low-esterified pectin exert healing and preventive effects on $CCL_4-induced$ hepatotoxicity in rats.