• Journal of Veterinary Clinics
• /
• v.30 no.1
• /
• pp.12-16
• /
• 2013

This study was performed to investigate hepatoprotective effect of rutin on acute hepatic damage induced by carbon tetrachloride in rats. Twenty-four male Sprague-Dawley rats were randomly divided into four groups; normal control group, $CCl_4$ control group, two rutin treatment groups (rutin 200+$CCl_4$ and rutin 400+$CCl_4$). Dissolving vehicles were applied to the rats in the normal control group. The rutin was administrated to the rats in rutin 200+$CCl_4$ and rutin 400+$CCl_4$ groups at the levels of 200 mg/kg and 400 mg/kg, 3 consecutive days orally, with 24 hours interval before inoculating $CCl_4$. $CCl_4$ was intraperitoneally administered an hour after the last treatment of rutin to the rats in every group except the normal control group. The body weight of rats in $CCl_4$ control group were significantly lower than other groups (p < 0.05), but the liver weight and relative liver weight were higher than normal control group (p < 0.05). The activities of ALT, AST, ALP, GTP, LDH and the level of total bilirubin in sera of rats in $CCl_4$ control group were higher and the levels of total protein, albumin and globulin were lower than the normal group (p < 0.05). The activities of ALT, AST, ALP, GTP, LDH and the level of total bilirubin in rutin 200+$CCl_4$ and rutin 400+$CCl_4$ groups were lower than $CCl_4$ control group (p < 0.05). Therefore the pre-treatment of rutin before $CCl_4$ inoculation in rats effectively inhibited the elevation of serum ALT, AST and total bilirubin which are the parameters of hepatic damage.

• YAKHAK HOEJI
• /
• v.54 no.1
• /
• pp.55-61
• /
• 2010

Gardenia jasminoides is one of the most widely used herbal preparations for the treatment of liver disorders. This study evaluated the potential beneficial effect of G. jasminoides in a mouse model of carbon tetrachloride ($CCl_4$)-induced liver injury. The mice were treated intraperitoneally with $CCl_4$ (10 ${\mu}l$/kg). They received G. jasminoides (30, 100, 300 mg/kg) 48 h, 24 h and 2 h before and 6 h after administering $CCl_4$. The serum activities of aminotransferase and the hepatic level of malondialdehyde were significantly higher 24 h after the $CCl_4$ treatment, while the concentration of reduced glutathione was lower. These changes were attenuated by G. jasminoides. $CCl_4$ increased the level of circulating tumor necrosis factor-$\alpha$ (TNF-$\alpha$) markedly, which was reduced by G. jasminoides. The levels of hepatic inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression were markedly higher after the $CCl_4$ treatment. G. jasminoides diminished these alterations. $CCl_4$ increased the level of TNF-$\alpha$, iNOS and COX-2 mRNA expressions, and these increases were attenuated by G. jasminoides. These results suggest that G. jasminoides alleviates $CCl_4$-induced liver injury, and this protection is likely due to the reduced oxidative stress and the downregulation of proinflammatory mediators.

• The Korea Journal of Herbology
• /
• v.36 no.1
• /
• pp.1-8
• /
• 2021

Objective : Citri Unshius Pericarpium (Citrus unshiu peel) has been used in Korean medicine to treat indigestion, vomiting, coughing and phlegm. This study investigated the hepatoprotective effect of ethanol extract of Citrus unshiu peel (CEE) in cadmium (CdCl2)-treated mouse model. Methods : CEE was dissolved in water and administered orally to mice once a day for 7 consecutive days. The mice were then exposed to a single intraperitoneal (i.p.) injection of cadmium (4 mg/kg body weight) to induce acute hepatotoxicity. At the end of the experiment, blood and liver tissue samples were collected, analyzed for alanine aminotransferase (ALT), aspartate aminotransferase (AST), and histopathological evaluation. Liver damage was assessed as the percentage of degenerative areas of the hepatic parenchyma, the number of degenerative hepatocytes, and the number of infiltrated inflammatory cells. Results : In cadmium-treated rats, pretreatment with CEE significantly reduced the serum ALT and AST levels associated with liver damage. Histopathologically, CEE prevented degenerative changes on the hepatic tissues including confluent necrosis, congestions and infiltration of inflammatory cells. CEE also reduced the elevation of oxidative stress markers (nitrotyrosine and 4-hydroxynonenal) and apoptosis markers (cleaved caspase-3 and cleaved PARP) positive cells. PARP protein expression in liver tissue was also restored by CEE. Conclusion : This study showed that CEE exerted antioxidant and anti-apoptotic effects against cadmium-induced liver injury. Thus, it can be concluded that CEE can be used to prevent liver damage caused by cadmium.

• Korean Journal of Clinical Laboratory Science
• /
• v.47 no.4
• /
• pp.251-258
• /
• 2015

Curcumin, a major polyphenolic compound of turmeric, is well known to prevent non-alcoholic steatohepatitis (NASH) related to obesity. The aim of the study was to investigate the effect of curcumin on hepatic fibrosis induced by carbon tetrachloride ($CCl_4$) in obese mice. $CCl_4$ was administrated in mice fed a normal diet (ND) or a high fat diet (HFD) for 7 weeks together with or without curcumin. It was conducted to examine for metabolic profiles, adipocyte size, and liver fibrosis by serum biochemistry, histology and immunohistochemistry. Also, Apoptosis of hepatic cells was determined by the TUNEL method. Treatment with curcumin significantly lowered the body weight, fasting glucose, serum AST and ALT, and decreased the adipocyte size, the number of macrophage and mast cells in adipose tissue, and collagen deposition in liver tissue in the HFD+$CCl_4$ group compared with the findings of the HFD+$CCl_4$ group. In contrast, treatment with curcumin on the ND+$CCl_4$ group did not show a significant difference except the body weight and mast cell number when compared with the ND+$CCl_4$ group. Furthermore, curcumin significantly reduced the number of parenchymal apoptotic cells, whereas it increased the number of non-parenchymal apoptotic cells, especially resembling an activated hepatic stellate cell in the liver. Taken together, this data suggests that curcumin might be an effective antifibrotic drug for the prevention of liver disease progression in obese mice. Thus, the development of curcumin as a therapy for obesity and liver fibrosis is supported.

• Food Science and Preservation
• /
• v.24 no.1
• /
• pp.107-115
• /
• 2017

The aim of this study was to investigate the hepatoprotecive effect of silk protein hydrolysates (SDH), which was prepared by acid hydrolysis, in rats. SDH itself did not exhibit any cytotoxic effect on hepatic tissues. SDH showed a protective effect on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity and liver damage. SDH effectively reduced AST (aspartate aminotransferase) and ALT (alanine aminotransferase), which are biomarkers for liver damage, in a dose-dependent manner. Malondialdehyde (MDA), a lipid peroxidation product, was significantly reduced by SDH. A high dose of SDH (2 g/kg) reduced t-BHP-induced MDA production by 40%. Glutathione (GSH), which is an endogenous antioxidant molecule, was effectively increased by SDH treatment. GSH content was enhanced by around 2.5-fold, compared with t-BHP control, upon SDH (2 g/kg) treatment. Lactate dehydrogenase (LDH), which is an enzyme released by cell cytotoxicity, was greatly increased by t-BHP, but significantly decreased by SDH treatment. Furthermore, hematoxylin and eosin (H&E) staining showed that SDH suppressed t-BHP-induced lesions in liver tissue. Taken together, SDH might be used as a protective agent against liver damage.

• Korean Journal of Veterinary Research
• /
• v.36 no.2
• /
• pp.313-325
• /
• 1996

Experiments were undertaken to examine the ability of selenium to protect against alcohol and/or paraquat-induced hepatotoxicity and to examine the additive effect between alcohol and paraquat. Protective effect against hepatotoxic functions was measured in serum from alcohol(15% v/v), paraquat(200ppm), alcohol and paraquat, and combination of sodium selenite(4ppm) in drinking water-fed guinea pigs ad libitum for 4 weeks. A total of 68 healthy 7-weeks-old male animals were assigned at random to 8 treatment groups(9~13 animals/group). Body and liver weight losses, and high serum concentrations in aspartate aminotransferase(AST), alanine aminotransferase(ALT, in only paraquat group), $\gamma$-glutamyltranspeptidase($\gamma$-GTP), cholesterol(Cho), creatinine, blood urea nitrogen(BUN), total bilirubin(TB), direct bilirubin(DB), total protein(TP), albumin and globulin as well as low values in alkaline phosphatase(ALP) and glucose were produced in a groups of alcohol or paraquat-fed. These values were not potentiated in a group given the combination of alcohol plus paraquat. Morphological changes in the liver were also observed in the alcohol or paraquat-fed group. Lipid droplet and cell swelling in the hepatocytes were observed in alcohol-fed guinea pig, especially Mallory's hyaline arounded hepatic vein. In the paraquat-fed guinea pig, lipid droplet, pyknosis and karyolysis were observed. When alcohol or paraquat was combined with selenium-fed, hyperplasia of Kupffer cell in liver were observed. However, the mean ALT, $\gamma$-GTP, Cho, BUN, TB, TP, albumin and globulin values were lower in groups given the combination of alcohol and/or paraquat plus selenium, compared with groups given alcohol and/or paraquat. Also, the ratio of liver weight to body weight and ALP values(exception of paraquat plus selenium group) were increased by selenium. These results suggest that an adequate selenium confers marked protection against alcohol and paraquat-induced hepatotoxicity.

• Biomolecules & Therapeutics
• /
• v.24 no.6
• /
• pp.650-658
• /
• 2016

Chronic alcohol consumption causes alcoholic liver disease, which is associated with the initiation of dysregulated lipid metabolism. Recent evidences suggest that dysregulated cholesterol metabolism plays an important role in the pathogenesis of alcoholic fatty liver disease. Ecklonia stolonifera (ES), a perennial brown marine alga that belongs to the family Laminariaceae, is rich in phlorotannins. Many studies have indicated that ES has extensive pharmacological effects, such as antioxidative, hepatoprotective, and antiinflammatory effects. However, only a few studies have investigated the protective effect of ES in alcoholic fatty liver. Male Sprague-Dawley rats were randomly divided into normal diet (ND) (fed a normal diet for 10 weeks) and ethanol diet (ED) groups. Rats in the ED group were fed a Lieber-DeCarli liquid diet (containing 5% ethanol) for 10 weeks and administered ES extract (50, 100, or 200 mg/kg/day), silymarin (100 mg/kg/day), or no treatment for 4 weeks. Each treatment group comprised of eight rats. The supplementation with ES resulted in decreased serum levels of triglycerides (TGs), total cholesterol, alanine aminotransferase, and aspartate aminotransferase. In addition, there were decreases in hepatic lipid and malondialdehyde levels. Changes in liver histology, as analyzed by Oil Red O staining, showed that the ES treatment suppressed adipogenesis. In addition, the ES treatment increased the expression of fatty acid oxidation-related genes (e.g., PPAR-${\alpha}$ and CPT-1) but decreased the expression of SREBP 1, which is a TG synthesis-related gene. These results suggest that ES extract may be useful in preventing fatty acid oxidation and reducing lipogenesis in ethanol-induced fatty liver.

• Preventive Nutrition and Food Science
• /
• v.13 no.4
• /
• pp.269-275
• /
• 2008

Dandelion (Taraxacum officinale) has been widely used as an anti-inflammatory agent in oriental medicine. In the current study, we investigated the protective effect, and the possible mechanism, of dandelion extracts against ethanol-induced acute hepatotoxicity in C57BL/6 mice. Dandelion water and ethanol extract was administered at 2 g/kg body weight (BW) once daily for 7 consecutive days, whereas control and ethanol groups received water by gavage. Ethanol (50% ethanol; 6 g/kg BW) was administered 12 hr before sacrificing the mice in order to generate liver injury. Significantly increased serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities as well as liver triglyceride (TG) and cholesterol levels were attenuated by dandelion supplementation. In addition, dandelion extracts not only enhanced alcohol dehydrogenase (ADH) and anti-oxidative enzyme activities, but reduced lipid peroxidation. Cytochrome P450 2E1 (CYP 2E1), one of the critical enzymes xenobiotic metabolism, expression was lower with ethanol treatment but restored by dandelion supplementation. These results were confirmed by improved histopathological changes in fatty liver and hepatic lesions induced by ethanol. In conclusion, dandelion could protect liver against ethanol administration by attenuating of oxidative stress and inflammatory responses.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.25 no.4
• /
• pp.620-627
• /
• 2011

We evaluated the hepatoprotective activity of crude hot-water extracts of the traditional Korean medicinal herb, Phellodendri Cortex (PC; Bark of Phellodendron amurense RUPR.), in an experimental model of hepatic damage induced by carbon tetrachloride ($CCl_4$). The serum marker of liver damage, sGOT, sGPT and sALP, were significantly decreased in the liver of the PC treated rats, compared with that of $CCl_4$ treated group. The histological observation of liver section of rats, showed the same protective effect of PC treatment. And the protective activity of PC was more significant in the post-treated group than pre-treated group. The significant decrease of malodialdehyde and increase of glutathion, catalase activity were observed in the liver homogenate of PC treated rats. Based on these findings, it is suggested that PC has potent hepatoprotective effects and the mechanism of the protection may be related to antioxidation pathways.

• Journal of The Korean Society of Clinical Toxicology
• /
• v.15 no.2
• /
• pp.107-115
• /
• 2017

Purpose: Glehnia littoralis has been used to treat ischemic stroke, phlegm, cough, systemic paralysis, antipyretics and neuralgia. The pharmacological mechanisms of Glehnia littoralis include calcium channel block, coumarin derivatives, anticoagulation, anti-convulsive effect, as well as anti-oxidant and anti-inflammatory effects. Alpha-amanitin (${\alpha}$-amanitin) is a major toxin from extremely poisonous Amanita fungi. Oxidative stress, which may contribute to severe hepatotoxicity was induced by ${\alpha}$-amanitin. The aim of this study was to investigate whether Glehnia littoralis ethyl acetate extract (GLEA) has the protective antioxidant effects on ${\alpha}$-amanitin -induced hepatotoxicity. Methods: Human hepatoma cell line HepG2 cells were pretreated in the presence or absence of GLEA (50, 100 and $200{\mu}g/ml$) for 4 hours, then exposed to $60{\mu}mol/L$ of${\alpha}$-amanitin for an additional 4 hours. Cell viability was evaluated using the MTT method. AST, ALT, and LDH production in a culture medium and intracellular MDA, GSH, and SOD levels were determined. Results: GLEA (50, 100 and $200{\mu}g/ml$) significantly increased the relative cell viability by 7.11, 9.87, and 14.39%, respectively, and reduced the level of ALT by 10.39%, 34.27%, and 52.14%, AST by 9.89%, 15.16%, and 32.84%, as well as LDH by 15.86%, 22.98%, and 24.32% in culture medium, respectively. GLEA could also remarkably decrease the level of MDA and increase the content of GSH and SOD in the HepG2 cells. Conclusion: In the in vitro model, Glehnia littoralis was effective in limiting hepatic injury after ${\alpha}$-amanitin poisoning. Its antioxidant effect is attenuated by antidotal therapy.