• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.87-91
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• 1989

Effect of ginseng butanol fractions on the hepatic mitochondrial monoamine oxidase activity with ethanol treatment was investigated in this experiment. Ethanol treatment, either acutely or chronically, increased the hepatic mitochondrial monoamine oxidase activity compared to control group. Whereas, treatment with ginseng butanol fractions lowered the ethaol-induced monoamine oxidase activity. Acetaldehyde, the major metabolite of ethanol, significantly increased the hepatic mitochondrial monoamine oxidase activity more than ethanol did. It was also observed that ginseng butanol fractions reduced the increase of the hepatic mitochondial monoamine oxidase activity by acetaldehyde. From these results, it is suggested that ginseng butanol fractions may be associated with the modulation of the hepatic mitochondrial monoamine oxidase activity in ethanol-treated animals.

• Biomolecules & Therapeutics
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• v.17 no.3
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• pp.318-324
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• 2009

1-Furan-2-yl-3-pyridin-2-yl-propenone (FPP-3) has recently been synthesized and characterized to have an anti-inflammatory activity through the inhibition of the production of nitric oxide. In the present study, adverse effects of FPP-3 on hepatic functions were determined in female BALB/c mice. When mice were administered with FPP-3 at 125, 250 or 500 mg/kg for 7 consecutive days orally, FPP-3 significantly increased absolute and relative weights of liver with a dose-dependent manner. In addition, FPP-3 administration dramatically increased the hepatotoxicity parameters in serum at 500 mg/kg, in association of hepatic necrosis. FPP-3 significantly induced several phase I enzyme activities. To elucidate the possible mechanism(s) involved in FPP-3 induced hepatotoxicity, we investigated the hepatic activities of free radical generating and scavenging enzymes and the level of hepatic lipid peroxidation. FPP-3 treatment significantly elevated the hepatic lipid peroxidation, measured as the thiobarbituric acid-reactive substance, and the activity of superoxide dismutase. Taken together, the present data indicated that reactive oxygen species might be involved in FPP-3-induced hepatotoxicity.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.18 no.2
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• pp.121-127
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• 2015

Purpose: To evaluate clinical and laboratory profile of Wilson's disease (WD) in children. Methods: This cross sectional study was conducted at Bangabandhu Sheikh Mujib Medical University Hospital. Bangladesh, over a period of 3 years. One hundred consecutive children of WD between 3 to 18 years of age were evaluated. Results: Mean age was $8.5{\pm}1.5years$. Male female ratio was 2:1. Ninety-one percent of patients were Muslim and 9% Hindu. A total of 53% cases of hepatic WD presented between 5 to 10 years of age and most of the neurologic WD manifested in 10-15 years age group. Sixty-nine children presented only with hepatic manifestations, 6 only with neurological manifestations, 14 with both hepatic and neurological manifestation, 10 children was asymptomatic and 1 patient presented with psychiatric features. WD presented as chronic liver disease (CLD) in 42%, CLD with portal hypertension in 34%, acute hepatitis in 20% and fulminant hepatic failure in 4% cases. Stigmata of CLD were found in 18% patients. Keiser-Fleischser ring was found in 76% total patients. Elevated serum transaminase was found in 85% cases, prolonged prothrombin time in 59% cases and hypoalbuminaemia in 53% cases. A total of 73% patients had low serum ceruloplasmin, basal urinary copper of >$100{\mu}g/day$ was found in 81% cases and urinary copper following penicillamine challenge of >$1,200{\mu}g/day$ was found in 92% cases. Conclusion: Majority of studied WD children presented with hepatic manifestation of which 76% presented with CLD. Any child presented with jaundice after the age of 3 years should be investigated for WD.

• Journal of Veterinary Clinics
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• v.32 no.5
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• pp.449-453
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• 2015

A 7-year-old spayed female Somali-cross cat was admitted with a 4-week history of anorexia, vomiting, weight loss, and lethargy. The cat was diagnosed with hepatic lipidosis. With intensive care and nutritional support via a nasogastric feeding tube for 3 weeks, the clinical signs of hepatic lipidosis were improved. However, skin lesions were found in the left and right scapular regions during the treatment that were suspected to be due to feline skin fragility syndrome (FSFS). Intensive wound healing therapy with granulated sugar, laser therapy, and a surgical flap was conducted. Skin lesions improved uneventfully without other clinical signs or recurrence of any skin lesion for a year. To our knowledge, this is the first report of a good prognosis in a hepatic disorder and concurrent FSFS.

• Korean Journal of Veterinary Research
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• v.34 no.3
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• pp.619-626
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• 1994

The purpose of present study was to examine pharmacological effect of Artemisia Iwayomogi methanol extract(AIME) on biochemical parameters(activities of AST, ALT, LDH, and ALP, contents of total bilirubin, total protein, albumin and A/G ratio in serum and levels of hepatic microsomal lipid peroxide and glucose-6-phosphatase activities) against hepatic injury by carbon tetrachloride($CCl_4$) in rats. Increased AST, ALT and LDH activities by $CCl_4$ were decreased in AIMS treatment group at 48 or 72 hours. Together, increased ALP activity by $CCl_4$ almost returned toward normal value in AIME treatment group at 72 hours. Serum total bilirubin contents increased to 87, 79 and 31% compared with normal group by $CCl_4$ which were decreased to 64, 42 and 26% in AIME treatment group at 24, 48 and 72 hours, respectively. Decreased contents of total protein and albumin, and A/G ratio by $CCl_4$ were recovered in AIME treatment group. Hepatic microsomal lipid peroxide levels(nmol malonic dialdehyde/100mg protein) increased to 140, 95 and 78% compared with normal group by $CCl_4$ which were decreased to 107, 74 and 65% in AIME treatment group at 24, 48 and 72 hours, separately. Hepatic microsomal glucose-6-phosphatase activities decreased to 60, 50 and 53% compared with normal group by $CCl_4$ at 24, 48 and 72 hours, respectively, which were increased at 72 hours in AIME treatment group. In conclusion, AIME enhanced the amelioration process from $CCl_4$-induced lipid peroxidation, degeneration of liver cell, and impairment of protein and bilirubin metabolisms.

• Herbal Formula Science
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• v.10 no.1
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• pp.1-11
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• 2002

From the 24 kinds of literature on the Consumptive disease, it can be concluded as follows. 1. The consumptive disease is the Imparement of deficiency type due to overstrain. it is a general term for these all symptom such as and Deficiency of primordial Qi and Essence of life and blood. 2. The excessive fire due to Yin-Deficiency and the injury of spleen-stomach is accounted much of the cause of Consumptive disease. 3. The main cause of the Hepatic asthenia are the Anger, Consumption and over-thinking. 4. The symptoms of the Consumptive disease are mainly caused by the functional disorder of Liver taking charge of tendons. storing and regulating blood, Heart being in charge of blood circulation. taking charge of mental activities. Spleen taking charge of muscles, transforting and transforming nutrients. Lung taking charge of skins and hairs, taking charge of respirations, Kidney taking charge of bones, storing essence of life. 5. The main symptoms of Hepatic asthenia are flaccidity of muscles and temeons which causes limited movement caused by muscular atonia and the loss of bightness of eyes. 6. The main treatments of Consumptive disease are the invigorating the Spleen-stomach and the invigorating the Kidney and storing essence of life. 7. The treatments of Hepatic asthenia are the moderating the middle and the nourishing the muscles and tendons.

• Biomolecules & Therapeutics
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• v.25 no.5
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• pp.504-510
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• 2017

Inhibitor of nuclear factor kappa-B kinase beta ($IKK{\beta}$) plays a critical role in cell proliferation and inflammation in various cells by activating $NF-{\kappa}B$ signaling. However, the interrelationship between peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) and $IKK{\beta}$ in cell proliferation is not clear. In this study, we investigated the possible role of $PPAR{\alpha}$ in the hepatic cell death in the absence of $IKK{\beta}$ gene using liver-specific Ikkb-null ($Ikkb^{F/F-AlbCre}$) mice. To examine the function of $PPAR{\alpha}$ activation in hepatic cell death, wild-type ($Ikkb^{F/F}$) and $Ikkb^{F/F-AlbCre}$ mice were treated with $PPAR{\alpha}$ agonist Wy-14,643 (0.1% w/w chow diet) for two weeks. As a result of Wy-14,643 treatment, apoptotic markers including caspase-3 cleavage, poly (ADP-ribose) polymerase (PARP) cleavage and TUNEL-positive staining were significantly decreased in the $Ikkb^{F/F-AlbCre}$ mice. Surprisingly, Wy-14,643 increased the phosphorylation of p65 and STAT3 in both Ikkb and $Ikkb^{F/F-AlbCre}$ mice. Furthermore, BrdU-positive cells were significantly increased in both groups after treatment with Wy-14,643. Our results suggested that $IKK{\beta}-derived$ hepatic apoptosis could be altered by $PPAR{\alpha}$ activation in conjunction with activation of $NF-{\kappa}B$ and STAT3 signaling.

• Journal of Yeungnam Medical Science
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• v.4 no.1
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• pp.89-96
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• 1987

Carbon tetrachloride and Dimethylnitrosamine, both potent hepatotoxic agents, affect the hepatic lobules with fatty changes and central necrosis, and hemorrhagic necrosis. To study the effects on morphologic changes of the hepatic lobules in cases of single and repeated treatment of both hepatotoxins, sublethal doses of carbon tetrachloride, 0.4ml/kg, and dimethylnitrosamine, 40mg/kg of rats were given intraperitoneally single, twice and triple. With interval of 3 days, and the results were as follows : 1. The fatty changes and central necrosis of the hepatic lobules were milder and more quickly disappeared in the rats with twice or triple treatment than single administration of carbon tetrachloride, and regenerative changes of hepatic and sinusoidal cells achieved fater in the rats with repeated administration of carbon tetrachloride than those with single treatment. 2. The hemorrhagic necrosis of the hepatic lobules was not significantly influenced by the times of DMN treatment, but the hyperplastic changes showed more active to animals, with multiple administration of DMN.

• Fisheries and Aquatic Sciences
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• v.6 no.2
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• pp.81-87
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• 2003

Experiments were carried out to investigate the accumulation and the histopathological changes in liver of juvenile rockfish, S. schlegeli, after sub-chronic dietary Cu (0, 50, 125, 250 and 500mg/kg) exposure for 60 days. Cu accumulation in liver was significantly increased with dietary exposure period and concentration for 60 days, and has a linear relation with dietary exposure days. After 60 days of Cu dietary exposure, the Cu concentration in the liver was $75.9\pm12.05,\;126.29\pm22.11\;and\;360.44\pm45.26\;{\mu}g/g$ dry weight and was approximately 11-fold, 18-fold and 51-fold higher than in the control diet group at 125, 250 and 500 mg/kg Cu diet group. The accumulation factors were increased with the dietary exposure period in liver of rockfish. In the primary exposed stage, the effect of hepatic tissue in the rockfish exposed to dietary Cu observed enlargement of hepatocytes nuclei, activity of hepatic cells and the swelling of hepatic cells. While exposed time and concentration were increased, the distinct granulation, irregular shape and necrosis of hepatic cells were observed. It was observed that granule degeneration and necrosis showed a part of cells in hepatic tissue after 60 days at 500 mg/kg.

• Nutrition Research and Practice
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• v.5 no.6
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• pp.520-526
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• 2011

Folate deficiency and hyperhomocysteinemia are found in most patients with alcoholic liver disease. Oxidative stress is one of the most important mechanisms contributing to homocysteine (Hcy)-induced tissue injury. However it has not been examined whether exogenous administration of folic acid attenuates oxidative stress and hepatic toxicity. The aim of this study was to investigate the in vivo effect of folic acid supplementation on oxidative stress and hepatic toxicity induced by chronic ethanol consumption. Wistar rats (n = 32) were divided into four groups and fed 0%, 12%, 36% ethanol, or 36% ethanol plus folic acid (10 mg folic acid/L) diets. After 5 weeks, chronic consumption of the 36% ethanol diet significantly increased plasma alanine transaminase (ALT) (P < 0.05) and aspartate transaminase (AST) (P < 0.05), triglycerides (TG) (P < 0.05), Hcy (P < 0.001), and low density lipoprotein conjugated dienes (CD) (P < 0.05) but decreased total radical-trapping antioxidant potential (TRAP) (P < 0.001). These changes were prevented partially by folic acid supplementation. The 12% ethanol diet had no apparent effect on most parameters. Plasma Hcy concentration was well correlated with plasma ALT (r = $0.612^{**}$), AST (r = $0.652^*$), CD (r = $0.495^*$), and TRAP (r = $-0.486^*$). The results indicate that moderately elevated Hcy is associated with increased oxidative stress and liver injury in alcohol-fed rats, and suggests that folic acid supplementation appears to attenuate hepatic toxicity induced by chronic ethanol consumption possibly by decreasing oxidative stress.