• Advances in Traditional Medicine
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• v.1 no.1
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• pp.89-96
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• 2000

A human hepatoma cell line, Hep G2 cells are a reliable for the study of alcohol-induced hepatotoxicity. In this study, the author investigated the effect of an aqueous extract of Asparagus $cochinchinensis_{MERRIL}$ (Liliaceae) roots (ACAE) on ethanol (EtOH)-induced cytotoxicity in Hep G2 cells. ACAE dose-dependently inhibited the EtOH-induced tumor necrosis $factor-{\alpha}\;(TNF-{\alpha})$ secretion. ACAE also inhibited the EtOH and $TNF-{\alpha}-induced$ cytotoxicity. Furthermore, the author found that ACAE inhibited the $TNF-{\alpha}-induced$ apoptosis of Hep G2 cells. These results suggest that ACAE may prevent the EtOH-induced cytotoxicity through inhibition of the apoptosis of Hep G2 cells.

• Journal of Haehwa Medicine
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• v.9 no.1
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• pp.135-142
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• 2000

For the evaluation of protective effect on hepatic damage by Korean red ginseng mixed formula, we used GR(Korean red ginseng), GRF-A(Korean red ginseng-mixed formula) as a materials. The study was performed on protective effect against hepatic damage induced by $CCl_4$. In vitro assay with 1.1 mM galactosamine, protection(%) was 44%(GR), 58%(GRF-A) at 50ug/ml, while maxium protection(%) was 5%(GR) and 24% (GRF-A) against acute hepatotoxicity by $CCl_4$. GRF-A significantly protected ethanol induced-liver damage by lowering ALT and ALP and fatty degenertion in liver tissue.

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.123.2-123.2
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• 2007

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• The Journal of Internal Korean Medicine
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• v.22 no.1
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• pp.87-93
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• 2001

A human hepatoma cell line, Hep G2 cells, is reliable for the study of alcohol-induced hepatotoxicity. The aim of this study is to determine the relationship between TNF-${\alpha}$, IL-$1{\alpha}$ production and EtOH-induced cytotoxicity on Hep G2 cells. The cells were incubated with EtOH in the presence of Artemisia Capillaris Herba(AC) for 24 hours and in the absence of AC for 48 hours. Cytoviability and cytokines release were analyzed by MTT assay and enzyme linked immunosorbent assay (ELISA), respectively. After 24 hours of EtOH exposure, the cytoviability had markedly decreased, and the release of cytokines had increased. The increased amount of cytokines contributed to EtOH-induced cytotoxicity. Anti-TNF-${\alpha}$ and IL-$1{\alpha}$ antibodies almost abolished it. Interestingly, EtOH-induced cytotoxicity and cytokines production were inhibited by AC. Moreover, when AC was used in combination with antibodies, there was a marked inhibition of EtOH-induced cytotoxicity. These results suggest that EtOH-induced cytotoxicity may regulate, by various factors, and AC may prevent the cytotoxicity through partial inhibition of the $TNF-{\alpha}$ and IL-$1{\alpha}$ secretion.

• CELLMED
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• v.2 no.4
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• pp.35.1-35.11
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• 2012

The homeopathic remedy Chelidonium majus 200C (Chel-200) is traditionally used by homeopathic practitioners in liver ailments arising out of hepatotoxicity. The present investigation was aimed at examining whether vitamin C (L-ascorbic acid or AA), used in both traditional and orthodox medicines, can show better effects when used in combination with Chel-200, in favorably modifying the toxicological effects induced by the chronic feeding of p-dimethylaminoazobenzene (p-DAB, initiator) and phenobarbital (PB, promoter) in mice for 7 days through 120 days to induce hepatotoxicity and liver tumors. Mice were euthanized at 7, 15, 30, 60, 90, and 120 days of carcinogen feeding to assess various cytogenetical, biochemical and histological changes occurring in them. In a placebo controlled study, Chel-200 or the respective placebo (Alcohol-200C or Alc, "vehicle" of homeopathic drug), was orally administered to toxicant-fed mice. Sub-groups of the mice receiving Chel-200 were also fed either AA or an Alc placebo and their individual and conjoint effects were studied against the respective controls, to evaluate if the combination therapy of Chel-200 with AA can be of additional help in the amelioration of the toxicities generated by the toxicants. The combined feeding of Chel-200 and AA appeared to reduce the cytotoxic and genotoxic effects significantly, when compared to either only the Chel-200 or AA fed group. A similar trend was also obtained in the results of scanning and transmission electron microscopic studies of the livers. Experiments in other mammalian models are warranted to confirm if these drugs in combination could be used in palliative care of human patients with liver diseases including cancer.

• 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.

• Journal of Preventive Medicine and Public Health
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• v.54 no.6
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• pp.471-480
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• 2021

Objectives: Cadmium is widely used, leading to extensive environmental and occupational exposure. Unlike other organs, for which the harmful and carcinogenic effects of cadmium have been established, the hepatotoxicity of cadmium remains unclear. Some studies detected correlations between cadmium exposure and hepatotoxicity, but others concluded that they were not associated. Thus, we investigated the relationship between cadmium and liver damage in the general population. Methods: In total, 11 838 adult participants from National Health and Nutrition Examination Survey 1999-2015 were included. Urinary cadmium levels and the following liver function parameters were measured: alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transferase (GGT), total bilirubin (TB), and alkaline phosphatase (ALP). Linear and logistic regression analyses were performed to assess the associations between urinary cadmium concentrations and each liver function parameter after adjusting for age, sex, race/ethnicity, annual family income, smoking status, alcohol consumption status, physical activity, and body mass index. Results: The covariate-adjusted results of the linear regression analyses showed significant positive relationships between log-transformed urinary cadmium levels and each log-transformed liver function parameter, where beta±standard error of ALT, AST, GGT, TB, and ALP were 0.049±0.008 (p<0.001), 0.030±0.006 (p<0.001), 0.093±0.011 (p<0.001), 0.034±0.009 (p<0.001), and 0.040±0.005 (p<0.001), respectively. Logistic regression also revealed statistically significant results. The odds ratios (95% confidence intervals) of elevated ALT, AST, GGT, TB, and ALP per unit increase in log-transformed urinary cadmium concentration were 1.360 (1.210 to 1.528), 1.307 (1.149 to 1.486), 1.520 (1.357 to 1.704), 1.201 (1.003 to 1.438), and 1.568 (1.277 to 1.926), respectively. Conclusions: Chronic exposure to cadmium showed positive associations with liver damage.

• 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.

• Korean Journal of Food Science and Technology
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• v.41 no.6
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• pp.706-711
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• 2009

Hepatoprotective effects of corn gluten hydrolysates (CGH) were investigated in rats orally treated with ethanol (30%(v/v), 3 g/kg body weight/day) for 4 weeks. Six-week old Sprague-Dawley male rats were divided into four dietary groups: normal diet (N), alcohol diet (E), E+CGH 1% diet (CGH-1%), and E+CGH 3% diet (CGH-3%). Body weights and liver indices were not significantly different among the four groups. However, food intakes were lower in the CGH groups than in the normal group (p<0.05). The administration of CGH significantly reduced serum alkaline phosphatase activity by 30% compared to the alcohol diet group. Among the antioxidative enzymes assessed, catalase activity was significantly decreased by 79% in the CGH diet groups compared to the alcohol diet group. In comparison to the alcohol-treated group, aldehyde dehydrogenase activity was increased by 20%, while microsomal ethanol oxidizing system activity was decreased by 20% in the CGH-treated groups. Furthermore, the area under the curve of the blood acetaldehyde concentration versus time profile after the administration of ethanol was significantly lower for the CGH rats than for the ethanol or asparaginic acid treated groups. Thus, CGH seems to offer beneficial effects by protecting against ethanol-induced hepatotoxicity by improving the acetaldehyde-related metabolizing system.

• Journal of Life Science
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• v.23 no.11
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• pp.1381-1387
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• 2013

The leaves and roots of Ligularia stenocephala, which are widely used as a food in Korea, were investigated for their antioxidant activities and cytotoxicity in vitro, and their hepatoprotective effect, alcohol detoxicant efficacy, and memory-enhancing property were investigated in vivo. The unique odor of the leaves was analyzed by GC-MS. Lipid peroxidation, superoxide anion formation, and DPPH radicals were inhibited remarkably by the extracts of the leaves and roots. The leaves of this edible plant significantly protected the hepatotoxicity induced by carbon tetrachloride and further diminished the blood alcohol content in mice. While the roots of this plant exhibited adequate cytotoxicity against four human tumor cell lines, especially against melanoma, the leaves revealed relatively weak activity. Both the leaves and the roots exerted an excellent ameliorating property on scopolamine-induced memory impairment in the passive avoidance task using an animal model. The hexane fraction of the leaves was analyzed by GC-MS, suggesting that a series of terpenoids may be odorous compounds in this plant.