• International Journal of Internet, Broadcasting and Communication
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• v.12 no.3
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• pp.131-138
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• 2020

The cabbage extract of the research does not show cytotoxicity, and thus can be used safely. In an experiment performed on an animal model with liver injury induced by a drug (APAP), it could be seen that the cabbage extract exhibited the effects of protecting liver and improving liver function by effectively reducing AST and ALT which are liver injury markers, indicating that the cabbage extract is effective as a pharmaceutical composition for preventing or treating liver disease. In particular, the cabbage extract was effective in treating inflammation of the liver by reducing the expression of the inflammatory mediators iNOS and COX-2 and the proinflammatory cytokine IL-1β, which are involved in acute inflammatory reactions accompanying liver injury. In the research, an extract of cabbage heat-treated at a temperature of 100 to 150℃ had a better liver function-improving effect or anti-inflammatory effect than an extract of raw cabbage.

• Nutrition Research and Practice
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• v.3 no.2
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• pp.95-101
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• 2009

It has been reported that dietary polyunsaturated fats (PUFA) increase liver injury in response to ethanol feeding. We tested the hypothesis that diets rich in linoleic acid (18:2n-6) would affect acute liver injury after acetaminophen injection and that protein restriction might exacerbate the liver injury. We examined effects of feeding diets with either 15% (wt/wt) corn oil or 14% beef tallow and 1% corn oil for six weeks with either 6 or 20 g/100 g protein on acute hepatotoxicity. After the feeding period, liver injury was induced by injecting either with 600 mg/kg body weight acetaminophen suspended in gum arabic-based vehicle, or with vehicle alone during fasting status. Samples of liver and plasma were taken for analyses of hepatic glutathione (GSH) levels and liver-specific enzymes [(Glutamate-pyruvate transaminase (GPT) and glutamate-oxaloacetate transaminase (GOT)], respectively. Whereas GSH level was significantly lower in only group fed 15% corn oil with 6 g/100 g protein among acetaminophen-treated groups, activities of GPT and GOT were significantly elevated in all groups except the one fed beef tallow with 20 g/100 g protein, suggesting low protein might exacerbate drug-induced hepatotoxicity. The feeding regimens changed the ratio of 18:2n-6 to oleic acid (18:1n-9) in total liver lipids approximately five-fold, and produced modest changes in arachidonic acid (20:4n-6). We conclude that diets with high 18:2n-6 promote acetaminophen-induced liver injury compared to diets with more saturated fatty acids (SFA). In addition, protein restriction appeared to exacerbate the liver injury.

• BMB Reports
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• v.38 no.3
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• pp.300-306
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• 2005

Tamoxifen citrate is an anti-estrogenic drug used for the treatment of breast cancer. It showed a degree of hepatic carcinogenesis, when it used for long term as it can decrease the hexose monophosphate shunt and thereby increasing the incidence of oxidative stress in liver rat cells leading to liver injury. In this study, a model of liver injury in female rats was done by intraperitoneal injection of tamoxifen in a dose of 45 mg/kg body weight for 7 successive days. This model produced a state of oxidative stress accompanied with liver injury as noticed by significant declines in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant elevations in TBARS (thiobarbituric acid reactive substance) and liver transaminases; sGPT (serum glutamate pyruvate transaminase) and sGOT (serum glutamate oxaloacetate transaminase) levels. The oral administration of dimethyl dimethoxy biphenyl dicarboxylate (DDB) in a dose of 200 mg/kg body weight daily for 10 successive days, resulted in alleviation of the oxidative stress status of tamoxifen-intoxicated liver injury in rats as observed by significant increments in the antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and catalase) and reduced glutathione concomitant with significant decrements in TBARS and liver transaminases; sGPT and sGOT levels. The administration of DDB before tamoxifen intoxication (as protection) is more little effective than its curative effect against tamoxifen-induced liver injury. The data obtained from this study speculated that DDB can mediate its biochemical effects through the enhancement of the antioxidant enzyme activities and reduced glutathione level as well as decreasing lipid peroxides.

• Journal of Acupuncture Research
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• v.26 no.5
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• pp.85-94
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• 2009

Objectives : This study was designed to investigate the effect of pharmacopuncture of Mori Cortex on galactosamine-induced liver injury in rats. Methods : Male Sprague-Dawley rats were divided into 5 groups; Normal, liver injury not induced and not treated group. Control, the liver injury-induced and not treated group. Saline group, the liver injury-induced and saline injection at $BL_{18}$. HA-1 and HA-2 group, the liver injury-induced and pharmacopuncture of Mori Cortex applied to $BL_{18}$, each $1.3{\mu}g/g$, $2.6{\mu}g/g$. Then we observed the changes of ${\gamma}$-GTP, GOT, GPT, LDH, total cholesterol, triglyceride, total bilirubin. Results : Pharmacopuncture of Mori Cortex treatment significantly inhibited the activities of ${\gamma}$-GTP, GOT, total cholesterol, triglyceride and total bilirubin in HA-1 group. ${\gamma}$-GTP, GTP, LDH, ${\gamma}$-GTP levels were significantly inhibited in HA-2 group. Conclusions : These results demonstrate that the reduce of hepatic enzyme activation and lipid accumulation by pharmacopuncture of Mori Cortex may be by an antioxidant properties of Mori Cortex.

• The Journal of Internal Korean Medicine
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• v.19 no.1
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• pp.22-38
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• 1998

This study was to investigate the hepatoprotective and anticirrhotic effects of Ganyeumilhobang(GIE) on the acute and chronic liver injury induced by various agents. Chronic liver injury induced by dimethylnitrosamine(DMN) ; a new experimental model for cirrhosis and the intraperitoneal injection of dimethylnitrosamine in the rat. Acute liver njury induced by carbon tetrachloride$(CCl_4)$ and D-galactosamine ; a experimental model for acute liver injury, the administration of $CCl_4$ and the intraperitoneal injection of D-galactosamine in the rat. The development of fibrosis and acute liver injury by the three prescriptions were examined by the chemical analysis of AST, ALT, prothrombin time and hydroxyproline. The results obtained were as follows. 1. The increasing level of hydroxyproline volume induced by DMN in mice was decreased by the oral administration of GIB. 2. The degree of histological fibrosis and hepatic inflammatory cell infiltration induced by $CCl_4$ decreased by the oral administration of GIB. 3. The increase of senun AST and ALT of mice with acute liver damage induced by $CCl_4$ and D-galactosamine was inhibited by the administration of GIB. 4. The prolongation of prothrombin time(seconds) of mice acute liver damage induced by $CCl_4$ was shortened by the oral administration of GIB. 5. The liver of mice was hepatectomized partial1y after the oral administration of GIB. The mitotic index(% of nuclei), weight of liver, contents of protein, RNA and DNA synthesis of the liver tissue were increased by the oral administration of GIB.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.1
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• pp.285-290
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• 2007

A liver is responsible for drug metabolism in a body. 10% of all medicine side effects lead to liver injury. Herb medicine is not an exception to this rule but all Herb medicines do not lead to liver injury absolutely. As for two times of occurrence of the drug induced liver injury during treatment of a CVA patient, we gave him Herb medicines in conjunction with Western medicines and Western medicines alone for each case. We meet with the result that giving the patient Herb medicines in conjunction with Western medicines reduces the duration of decreasing AST, ALT level as compared with giving him Western medicines alone. So we are now reporting the result.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.174-187
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• 2002

Objectives : This study was carried out to determine whether Kamihaengche-tang plus Yulanijihwang-tang (KCYH) exerts a protective effect against oxidant-induced liver cell injury. Methods : Cell injury was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. Results : Oxidants (tBHP and $H_2O_2$) increased dose-dependently LDH release which was significantly prevented by 1% KCYH. The protective effect of KCYH against oxidant-induced cell injury was dose-dependent in the range of 0.05-1 % concentrations. Similarly, KCYH inhibited oxidant-induced lipid peroxidation in a dose-dependent manner. When liver tissues were exposed to Hg (0.5 mM), ALT activity in the medium and lipid peroxidation in tissues were markedly increased. These changes were prevented by 1% KCYH, KCYH restored toxicant-induced inhibition of cellular GSH content. KCYH increased the activities of catalase and glutathion peroxidase in oxidant-treated tissues. Conclusions : These results indicate that KCYH exerts a protective effect against oxidant-induced liver cell injury, and this effect is attributed to prevention of lipid peroxidation. These effects may be due to an increase in concentration of endogenous antioxidants.

• Journal of Life Science
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• v.8 no.4
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• pp.464-471
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• 1998

This study was carried out to determine whether Kamihaengche-tang plus Yukmijihwang-tang (KCYH) exerts the protective effect against oxidant-induced liver cell injury. Cell injurt was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. $H_2O_2$increased LDH release which was significantly prevented by 1% KCYHT. The protective effect of KCYH against $H_2O_2$-induced cell injury was dose-dependent in the range of 0.05-1% concentrations. Similary, KCYH inhibited $H_2O_2$ induced lipid peroxidation in a dose-dependent manner. When liver tissuse were exposed to Hg(0.5 mM), ALT activity in the medium and lipid erpoxidation in tissues were markedly increased. These changes were prevented by 1% KCYH. KCHY restored Hg-induced inhibition of cellular GSH content. These result indicate that KCYH exerts the protective effect oxidant-induced liver cell injury, and this effect is attributed to prevented to prevention of lipid peroxidation. These dffects may be due to an increase in concentration of endogenous antioxidants.

• Journal of Korean Physical Therapy Science
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• v.8 no.1
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• pp.923-934
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• 2001

In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total body surface area 30%) except for inhalated injury. At 5 and 24 h after scald bum, biochemical assay and morphological changes in skin tissue, serum and liver tissue were examined. The effects of bum injury on the levels of glutathione, lipid peroxide and on the activities of oxygen free radical generating and scavenging enzymes have been determined in association with observing of histologic and ultrastructural changes, measuring the protein concentration in plasma, and counting the number of intravascular polymorphonuclear leukocytes. The activity of xanthine oxidase, an enzyme of oxygen free radical generating system. was elevated (p<0.01) in serum, but not in skin and in liver tissue. Futhermore, thermal injury decreased not only the protein concentration in plasma but also the number of leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.

• The Journal of Internal Korean Medicine
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• v.25 no.3
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• pp.539-544
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• 2004

Herbal medicine has been used in the Eastern world for 2,000 years, and is beneficial for numerous diseases. There have been reports pertaining to the safety of herbal medicine, but there have been few reports about herbal medicine induced liver injury in Eastern or Western medicine. Most are descriptions of hepatotoxicity of certain toxic herbs. We experienced one case of drug induced liver injury in the treatment of cerebral infarction with Chungsim Yeonja-tang. Although the patient had not used medication and Chungsim Yeonja-tang has no toxic herbs in it. patient's ALP, AST, ALT, GGT was twice elevated after 20 days on medication. This was diagnosed as drug induced liver injury, possibly due to incorrect diagnosis of Sasang constitution. So no herbal medicine was given for seven days. Then Gagam Saeng Gan-tang was given. Gagam Saeng Gan-tang have been used to treat hepatic disease and have been known to have beneficial effects. After 25 days on medication, the clinical symptoms and liver function improved. So, this case is presented to bring more attention to the toxicity of herbal medicines.