• The Journal of Korean Medicine
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• v.17 no.2 s.32
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• pp.251-263
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• 1996

In order to investigate experimentally that effect of Moschus, Bovis Calculus, Ursi Fel aqua-axupuncture on acutely damaged liver of rats induced by radix aconiti. The author admininisterated aqua-acupuncture according to method of manufacture stimulation to corresponding points, Kan-su$(BL_8)$ and Ki-mun($LR_{14}$), and carried out hematological, serological examination and electromicroscopical obseration. WBC level was decreased significantly in the experimental groups at 24 and 48 hours as compared with the control group. ${\gamma}-GTP$ level was decreased significantly in the experimental groups at 24 and 48 hours as compared with the control group. GPT level was decreased significantly in the experimental groups at 24 and 96 hours as compared with the control group, but GOT level did not reeveal any statistical difference. At 24-hours group, the cell organelles of the hepatic cells are destructed. The cisternae of the smooth endoplasmic reticulum are particulary dilated in the 24-hours control group compared with experimental group. At 48-hours group, the destructed cell organelles are recovered in the experimental group compared with control group. At 96-hours group, the cell organelles of hepatic cells are showing feture of normal group. According to the above findings, it is considered that Moschus, Bovis Calculus, Ursi Fel aqua-acupuncture has effects of recovery of acutely damaged liver.

• Molecules and Cells
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• v.46 no.8
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• pp.496-512
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• 2023

A fructose-enriched diet is thought to contribute to hepatic injury in developing non-alcoholic steatohepatitis (NASH). However, the cellular mechanism of fructose-induced hepatic damage remains poorly understood. This study aimed to determine whether fructose induces cell death in primary hepatocytes, and if so, to establish the underlying cellular mechanisms. Our results revealed that treatment with high fructose concentrations for 48 h induced mitochondria-mediated apoptotic death in mouse primary hepatocytes (MPHs). Endoplasmic reticulum stress responses were involved in fructose-induced death as the levels of phosho-eIF2α, phospho-C-Jun-N-terminal kinase (JNK), and C/EBP homologous protein (CHOP) increased, and a chemical chaperone tauroursodeoxycholic acid (TUDCA) prevented cell death. The impaired oxidation metabolism of fatty acids was also possibly involved in the fructose-induced toxicity as treatment with an AMP-activated kinase (AMPK) activator and a PPAR-α agonist significantly protected against fructose-induced death, while carnitine palmitoyl transferase I inhibitor exacerbated the toxicity. However, uric acid-mediated toxicity was not involved in fructose-induced death as uric acid was not toxic to MPHs, and the inhibition of xanthine oxidase (a key enzyme in uric acid synthesis) did not affect cell death. On the other hand, treatment with inhibitors of the nicotinamide adenine dinucleotide (NAD)⁺-consuming enzyme CD38 or CD38 gene knockdown significantly protected against fructose-induced toxicity in MPHs, and fructose treatment increased CD38 levels. These data suggest that CD38 upregulation plays a role in hepatic injury in the fructose-enriched diet-mediated NASH. Thus, CD38 inhibition may be a promising therapeutic strategy to prevent fructose-enriched diet-mediated NASH.

• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.6
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• pp.981-985
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• 1996

To study the effect of toluene administration on the liver damage, rats were previously fed a low (casein 7%, LP) or standard(casein 20%, SP) protein diet and for four days toluene(50% in olive oil) was given at 0.2ml/100g body weight/day to the male rats, and then the degree of liver damage in toluenetreated animals fed LP were compared with those fed SP. The increasing rate of liver weight/body weight and the serum levels of xanthine oxidase to the control group were higher in rats fed SP than those fed LP. The decreasing rate of protein contents in cytosol, mitochondria and glycogen, glutathione contents of liver to the control group were higher in rats fed SP than those fed LP. In histopathological findings, the swelling of hepatic cell around the central vein was demonstrated in all the two groups toluene-treated rats. But the degree of swelling severity in hepatocytes was somewhat higher in rats fed SP than those fed LP. Therefore it is assumed that the degree of liver damage severity in toluenetreated animals was higher in rats fed SP than those fed LP.

• KSBB Journal
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• v.23 no.5
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• pp.381-386
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• 2008

Lipophilic ammonia is toxic gas and can easily diffuse across cell membranes. Excess ammonia is implicated in the pathogenesis of several metabolic disorders including hepatic encephalopathy and may result in the death. The purpose of this study was to clarify the inhibition effect of metronidazole on liver cell damage due to ammonia in human Hep G2 cell and rat hepatocytes. The effects of metronidazole were studied in ammonium chloride treated human Hep G2 cell (75 mM) and rat hepatocyte (100 mM) following $0.1{\mu}M$ metronidazole treatment. In MTZ+AC group, cell viabilities increased prominently and LDH activities decreased over 25% than AC group. Furthermore, ammonia level according to ammonium chloride treatment reduced over 30% and lipid peroxidation as an index of cell membrane damage decreased more than twice. By comparison with control, catalase activity showed more than 30% reduction in AC group while less than 10% reduction in MTZ+AC group, respectively. In addition, MTZ+AC group showed the similar cell structure as control in cell morphology study by using light microscope, and represented fluorescent intensity decrement compared with AC group in fluorescent microscopic study with avidin-TRITC fluorescent dye. And cleaved PARP expression due to ammonia reduced twofold or more in MTZ+AC group. As the results suggest, metronidazole may protect the liver cell by inhibiting cell damages due to ammonia and be used for an effective antagonist of ammonia in hyperammonemia.

• Journal of the East Asian Society of Dietary Life
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• v.11 no.4
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• pp.259-267
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• 2001

This study was to investigate the effect of selenium on hepatic antioxidative defense system and oxidative damage in lead-administered rats. Male Sprague-Dawley rats weighing 140$\pm$5g were divided into one normal group(Se, 0 ppm) and three lead groups according to dietary levels of selenium supplementation: Pb0(Se, 0 ppm), PbS(Se, 0.5 ppm), and PbSS(Se, 1.0 ppm). All experimental groups were fed the experimental diet ad libitum for 4 weeks, and lead groups fed one containing 2,000 ppm lead acetate. Liver superoxide dismutase(SOD) activities in Pb0 group increased compared with other experimental groups. Liver gluthathione peroxidase(GSH-px) activities in Pb0 group decreased compared with normal group, but those of PbS and PbSS groups significantly increased compared with Pb0 group. Glutathione S-transferase(GST) activities decreased in Pb0 group and not significantly different from PbS and PbSS groups compared with normal group. Reduced glutathione(GSH) contents and GSH/GSSG of liver in Pb0 group were lower than those of other groups. Liver vitamin E contents in Pb0 group were about 50% of the normal group, but those of PbSS and PbS increased more than Pb0 group. Liver damage in electron microphotography process decreased in RER, showed an increase in Iysosome and also an increase in swelling of mitochondria. and ordered as follows : PbSS. PbS. and Pb0. It was concluded that high levels of dietary selenium had protective effects on peroxidative damage of hepatic cell accompanied with increased antioxidative defense system in lead-administered rats.

• Korean Journal of Food Science and Technology
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• v.31 no.3
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• pp.831-837
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• 1999

Ochratoxin A (OA), a naturally occurring mycotoxin, has been known to cause renal and hepatic lesion in human and animals. This study was carried out to investigate the modulation effects of antioxidant vitamins on OA-induced lipid peroxidation associated with oxidative damage. Vitamin C (10 mg/kg/day) and vitamin E (63.8 mg/kg/day) were administered by intraperitoneal (i.p.) injection to male ICR mice, and 1 hr later, OA which was dissolved in 0.1 M $NaHCO_3$, treated 4 mg/kg/day by i.p. injection. During 4 days repeated, and then measured superoxide dismutase (SOD) activity, catalase activity and malondialdehyde (MDA) formation in microsomes of liver and kidney. Additionally, the relationship between cell damage and modulation effects of antioxidant vitamins was evaluated by comet assay. Results were as followed; i) SOD, catalase activity and MDA level were significantly increased by OA treated, ii) SOD, catalase activity and MDA formation were significantly decreased by antioxidant vitamins combine treated, iii) blood cell damage associated with lipid peroxidation, induced by OA, also modulated by antioxidant vitamins. These results indicated that antioxidant vitamins might be used for prevention of renal and hepatic damage due to ochratoxicosis.

• Journal of Nutrition and Health
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• v.33 no.2
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• pp.124-133
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• 2000

This study evaluated the effects of chronic ethanol consumption and/or taurine supplementation on hepatic total, phospholipid fatty acid composition and the metabolism of rats fed one of three purified liquid diets for 8 weeks. the rats followed either the control diet (CD, ethanol-free and taurine-free diet); ethanol diet (ED, CD+ 50g ethanol/L) or ethanol-taurine diet (ETD, ED+3.75g taurne/L). Chronic ethanol consumption and/or dietary taurine supplementation were associated with altered hepatic total and phospholipid fatty acid composition. compared to the values for the control rats, ED or ETD significantly decreased the percentage of total monounsaturated fatty acids ($\Sigma$MUFA), and increased the percentage of total polyunsaturated fatty acids ($\Sigma$PUFA) of hepatic total lipids(p〈0.01). Percentages of 14:0(P〈0.01) and 16:0(p〈0.001) were sigificantly lower, and those of 18:0(p〈0.01), 20:0(p〈0.001), 20:3$\omega$6(p〈0.01) and 22:4$\omega$6(p〈0.01) in hepatic total fatty acid compositions were oserved in rats fed ETD versus those fed ED or ETD. No significant differences in hepatic total fatty acid compositions were observed in rats fed ETD versus those fed ED. Percentages of 24:0(p〈0.01), 16:1(p〈0.05), 20:1(p〈0.01), 18:2$\omega$6(p〈0.01) and 18:3$\omega$3(p〈0.05) in hepati phospholipids were significantly higher, and those of 14:0(p〈0.01), 16:0(p〈0.001), 20:3$\omega$3(p〈0.05) in hepatic phospholipids were significantly higher, and those of 14:0(p〈0.01), 16:0(p〈0.001), 20:3$\omega$3(p〈0.001), 22:6$\omega$3(p〈0.001) and $\Sigma$$\omega$3(P〈0.001) were significantly lower in rats fed ED or ETD compared to the values for the control rats. The Δ5 desaturation index(20:3$\omega$6⇒20:4$\omega$6) and elongation index (20:5$\omega$3⇒22:5$\omega$3) of hepatic phospholipid index (20:3$\omega$6⇒20:4$\omega$6) and decreased Δ4 desaturation index (22:5$\omega$3⇒22:6$\omega$3) compared to the values for the ED rats. These changes in hepatic fatty acid composition induced by chronic ethanol consumption and/or taurine supplementation might be associated with the modulations of physical properties of the hepatic cell membrane and its sensitivity to peroxidation damage.

• Journal of Ginseng Research
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• v.36 no.3
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• pp.248-255
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• 2012

Potential antioxidant effect of processed ginseng (sun ginseng, SG) on oxidative stress generated by tert-butyl hydroperoxide (t-BHP) was investigated in HepG2 cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase (LDH) leakage test demonstrated that SG dose-dependently prevents a loss of cell viability against t-BHP-induced oxidative stress. Also, SG treatment dose-dependently relieved the increment of activities of hepatic enzymes, such as aspartate aminotrasferase and alanine aminotransferase, and lipid peroxidation mediated by t-BHP treatment in HepG2 cells. SG increased the gene expression of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. However, high dose of SG treatment caused decrease in mRNA level of glutathione peroxidase as compared to low dosage of SG-treated cells. The gene expression of glutathione reductase was found to be slightly increased by SG treatment. In addition, SG extract attributed its hepaprotective effect by inducing the mRNA level of bcl-2 and bcl-xL but reducing that of bax. But, the gene expression of bad showed no significant change in SG-treated HepG2 cells. These findings suggest that SG has hepatoprotective effect by showing reduction of LDH release, activities of hepatic enzymes and lipid peroxidation and regulating the gene expression of antioxidant enzymes and apoptosis-related molecules against oxdative stress caused by t-BHP in HepG2 cells.

• The Journal of Korean Medicine
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• v.18 no.1
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• pp.430-445
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• 1997

In order to know the effects of Calculus $Bovis{\cdot}F디$ Ursi aqua-acupuncture ($C{\cdot}F$ aqua-acupuncture) to the liver damage, we carried out the treatment of $C{\cdot}F$ aqua-acupuncture and injection of Kam-Du-Tang on the liver damaged rat which is induced by aconitine, and then ultrastructural study has been to the liver tissue. The results were as follows: 1. In the hepatic cell of normal group, the nuclear envelope is round and electro-density of nucleoplasm is relatively low, and have one or two large nucleolus. Cell organelle is developed rough endoplasmic reticulum(RER) and many mitochondria, glycogen granules, smooth endoplasmic reticulum(SER) and Golgi apparatus. 2. In 24 hours control group, nuclear envelope is very irregular, RER and most of cell organell is shown that destroyed by aconitine. This is similar to the 48 hours control group. In 72 hours control group, RER is recovered somewhat but cristae of mitochondria is not seen the shape 3.In 24 hours $C{\cdot}F$ aqua-acupuncture group, nuclear envelope is very irregular and cristernae is very dilatable and many mitochondria is dilationed and the cristae is not definite like the control group. In 48 hours $C{\cdot}F$ aqua-acupuncture group, nuclear envelope is relatively round and chromatin is regular. Cristernae of RER and ribosme is somewhat imperfect but is similar the normal group, and the cristae of mitchondria is shown definitely like the normal group. In 72 hours $C{\cdot}F$ aqua-acupuncture group, nuclear envelope is round and cell organell is similar to normal group. 4. In 24 hours Kam-Du-Tang group, nuclear envlope is very irregular and cell organelles are destroyed by the effects of aconitine. In 48 hours Kam-Du-Tang group, nuclear envelope is somewhat irregular but chromatin is relatively regular. RER is seperated regularly through the cytoplasm, but cannot make the structure of lamina, and cistennae is very dilationed. many of glycogen granules is seperated regularly. In 72 hours Kam-Du-Tang group, RER makes the lamina. Mitochondria is a little but inner space is dilationed so the shape of is not definite and a lot of glycogen granules are accumulated in several places. It see the above result, hepatic cell that is damaged by aconitine is effected chiefly by the $C{\cdot}F$ acupuncture and effect of acupuncture is similar to the detoxicated effect of Kam-Du-Tang.

• Herbal Formula Science
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• v.10 no.2
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• pp.127-141
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• 2002

Objectives: Haeganjeon(HGJ) has been used for the treatment of liver disease in traditional medicine. The present study was carried out to evaluate the antioxidant and protective effects of HGJ extract on oxidative damage of hepatocytes by tert-butyl hydroperoxide(t-BHP). Methods: In the linoleic acid water-alcohol system, the levels of lipid peroxide(LPO) were determined by TBA method. The scavenging effect of HGJ on ${\alpha},{\alpha}-diphenyl-{\beta}-picrylhydrazyl$(DPPH) radical was determined according to the method of Hatano. In the Fenton system(ferrous ion reaction with hydrogen peroxide), the levels of hydroxyl radical induced LPO in rat liver homogenate were determined according to the method of TBA. Inhibitory effect of HGJ on superoxide generation was measured by xanthine-xanthine oxidase system. In order to evaluate antioxidative activity of HGJ in the liver cell, cultured normal rat liver cells(Ac2F) were prepared and incubated with or without HGJ. After 18hr, cells placed in DMEM medium without serum, and then incubated with 1mM tert-butyl hydroperoxide(t-BHP) for 2hrs. Viable cells were detected by MTT assay. Conclusions: In the linoleic acid autoxidation system, HGJ extract significantly inhibited the time course of the lipid peroxidation. These effects were similar to those of BHA HGJ extracts showed about 70% scavenging effect on DPPH radical. And HGJ extract inhibited the lipid peroxide formation in rat liver homogenate induced by hydroxyl radical derived from Fenton system. In addition, HGJ extract protected the cell death induced by t-BHP and significantly increased cell viability in the normal rat liver cell. These result indicated that HGJ extract might playa protective role against oxidative hepatic cell injury by means of free radical scavenger.