• The Korean Journal of Physiology and Pharmacology
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• v.4 no.2
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• pp.121-127
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• 2000

Intracellular accumulation of bile acids in the hepatocytes during cholestasis is thought to be pathogenic in cholestatic liver diseases. The objective of this study was to determine the role of lipid peroxidation and glutathione on the bile acid-induced hepatic cell death mechanism in primary cultured rat hepatocytes. To induce hepatic cell death, we incubated primary cultured rat hepatocytes with glycochenodeoxycholic acid $(GCDC;\;0{\sim}400\;{\mu}M)$ for 3 hours. In electron microscopic examination and agarose gel electrophoresis, low concentration of GCDC treatment mainly induced apoptotic feature. Whereas $400\;{\mu}M$ GCDC treated cells demonstrated both apoptosis and necrosis. Lipid peroxidation was increased dose-dependently in GCDC treated hepatocyte. And this was also accompanied by decreased glutathione. Therefore, oxygen free radical damage may play a partial role in GCDC-induced hepatic cell death.

• The Journal of Dong Guk Oriental Medicine
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• v.6 no.1
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• pp.107-115
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• 1997

Hapatic tissues of ICR mouse intraperitoneally injected with Triton WR-1339 were observed to investigate the morphologic change of liver by destruction of lipid metabolism as hyperlipidemia. The hepatic tissues were obtained at hour-24, 48, and 72 after triton injection that were fixed in fromol-calcium solution and were cryocut. These tissues were stained by H&E for general morphology, sudan black B for lipid, and perchloric acid-naphthoquinone method for cholesterol. The increase of hepatocyte having meshlike cytoplasm were shown in all hepatic lobules after triton injection and the hepatic plates were disappeared in the region aggregated meshlike hepatocyte. The number of blue black colored lipid drop and dark green colored asterisk shaped cholesterol particle in hepatic cytoplasm were increased than the saline injected mouse and the size of lipid drop was enlarged. As results indicated that the lipid metabolism were destructed by triton injection, subsequently hepatocyes accumulated with lipid including cholesterol.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.5
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• pp.750-756
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• 1994

The effect of onion juice on ethanol -induced lipid peroxidation were studied were studied in rats. The contents of thiobarbituric acid (TBA) -reactants increased significantly in liver thanol(4ml/kg/day) administered -rats. The activities of serum alanine aminotransferase and alkaline phosphatase increased by ethanol administration compared with control group, but alterations of antioxidant enzymes activities in liver of ethanol administered rats were not significant vs control group. The glutathione contents in liver decreased by ethanol , whereas the glutathione level increased in ethanol and onion juice group compared with ethanol group. The contents of hepatic TBA-reactants and serum aminotrasnferase activity in ethanol group were reduced by onion juice administration. In these results, increased hepatic TBA-reactants of liver in ethanol group might be due to decreased glutathione contents in liver. Reduced glutathione (GSH) plays an important roles in the liver in several detoxification and the reduction of lipid peroxides. So the protective effects of onion juice on ethanol-induced increment of TBA-reactants may be due to the increament of lgutathions content. The glutathione depletion by ethanol was an important factor of ethanol-induced cell damage, and the prevention of onion juice to the glutathione depletion reduced by ethanol may be an important factor on the protection from ethanol-induced lipid perpxidation in rats.

• Journal of Nutrition and Health
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• v.26 no.5
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• pp.558-565
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• 1993

This study was carried out to observe the effects of dietary n-6, n-3 fatty acids and vitamin A levels on serum lipid contents and hepatic tissues in rats. Sixty eight male Sprague-Dawley rats were fed 6 different experimental diets for 6 weeks. The diets were composed of 10% of either corn oil or fish oil with three levels of vitamin A ; defient (1240IU/kg diet), adequate (4000IU/kg diet), excess(400,000IU/kg diet). It was observed that triglyceride content and lipoprotein ratio in serum were not affected by dietary fat types and vitamin A levels. However, total serum cholesterol contents were significantly lower in fish oil groups than in corn oil groups, which were not affected by vitamin A levels. Under light microscope, vitamin A excess groups showed pathological abnormalites, such as fatty change and inflammation of the hepatic tissues. There abnormalities were less severe in fish oil groups. These results suggested that fish oil could be a dietary factor lowering the serum lipid contents, and it seems to relieve the abnormal changes in liver induced by excess vitamin A.

• Journal of Nutrition and Health
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• v.41 no.4
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• pp.299-306
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• 2008

The purpose of this research was to investigate the effect of the calcium intake on lipid profile and antioxidant capacities in ovariectomized (OVX) rats. Rats were divided into 3 groups and fed diet with different levels of calcium (low 0.1%, adequate 0.5%, high 1.5%) for 4 weeks. The half of rats in each group was ovariectomized and the others were sham-operated. And rats were fed same diets for 8 weeks after operation. Feed intake and weight gain were significantly higher in OVX group than those in sham-operated. Serum HDL-cholesterol was the highest in high-calcium group of OVX. Hepatic triglyceride of low-calcium group in sham-operated was the highest, while that of highcalcium group in OVX was the highest. Hepatic activities of glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px), and catalase were significantly decreased by increasement of calcium intake. Hepatic TBARS level was the lowest in high-calcium group of OVX. And hepatic level of TBARS induced by AAPH was significantly decreased by increasement of calcium intake. These results may indicate that the high calcium intake have the potential role to improve lipid profiles and antioxidant capacities in OVX rats.

• Natural Product Sciences
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• v.20 no.1
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• pp.65-70
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• 2014

This study was carried out to investigate the potential effects of Gardenia jasminoides (GJ) extracts, on hepatic steatosis and lipid metabolism in mice fed with high-fat diet (HFD). GJ extracts (100 mg/kg, ${\times}10$ weeks) fed mice showed reduced body weight, adipose tissue weight, reduced aminotransferase level in plasma and hepatic lipid (triglyceride, total cholesterol) content. These effects were accompanied by decreased expression of lipogenic genes, sterol regulatory element binding protein-1c (SREBP-1c), liver X receptor (LXR), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), cluster of differentiation 36 (CD36), lipoprotein lipase (LPL) and decreased lipogenic enzyme FAS and HMG-CoAR enzyme activities while elevating carnitine palmitoyltrasferase-1 (CPT) activity. Based on these results, we speculated that the inhibitory effect on hepatic steatosis of GJ extract containing geniposide is the result of suppression of lipid synthesis in mice fed with HFD, suggesting that GJ extract may be beneficial in preventing hepatic steatosis.

• Journal of Microbiology and Biotechnology
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• v.23 no.11
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• pp.1569-1576
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• 2013

In mice, supplementation of t10,c12 conjugated linoleic acid (CLA) increases liver mass and hepatic steatosis via increasing uptake of fatty acids released from adipose tissues. However, the effects of t10,c12 CLA on hepatic lipid synthesis and the associated mechanisms are largely unknown. Thus, we tested the hypothesis that gut microbiota-producing t10,c12 CLA would induce de novo lipogenesis and triglyceride (TG) synthesis in HepG2 cells, promoting lipid accumulation. It was found that treatment with t10,c12 CLA ($100{\mu}M$) for 72 h increased neutral lipid accumulation via enhanced incorporation of acetate, palmitate, oleate, and 2-deoxyglucose into TG. Furthermore, treatment with t10,c12 CLA led to increased mRNA expression and protein levels of lipogenic genes including SREBP1, ACC1, FASN, ELOVL6, GPAT1, and DGAT1, presenting potential mechanisms by which CLA may increase lipid deposition. Most strikingly, t10,c12 CLA treatment for 3 h increased phosphorylation of mTOR, S6K, and S6. Taken together, gut microbiota-producing t10,c12 CLA activates hepatic de novo lipogenesis and TG synthesis through activation of the mTOR/SREBP1 pathway, with consequent lipid accumulation in HepG2 cells.

• The Journal of Internal Korean Medicine
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• v.33 no.3
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• pp.306-316
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• 2012

Objectives : Mori Folium is used for hyperlipidemia or diabetes. The study was designed to test the anti-obesity effect of Mori Folium on body weight, hepatic fat accumulation and serum lipid level. Methods : The extract from Mori Folium was made by the pharmacy department of Kyung-hee oriental medical hospital. Normal diet, high-fat diet, 30% reduced diet and Mori Folium groups were set. The normal group was administered normal rat food, but the other three groups were administered high fat food. We measured body weight once a week. After 3 weeks experiment, hepatic lipid accumulations were measured. Also we compared serum lipid levels among the 4 groups after 3 weeks. Results : Mori Folium had no effect on body weight, but the 30% reduced diet had an inhibitory effect on body weight gain. Mori Folium had more inhibitory effect on hepatic fat accumulation than a 30% reduced diet. Mori Folium also has more inhibitory effect on serum triglyceride than 30% reduced diet. Conclusions : Mori Folium has anti-obesity effect on hepatic lipid accumulaion and serum triglyceride level in high fat diet induced rats.

• Journal of Society of Preventive Korean Medicine
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• v.22 no.2
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• pp.77-107
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• 2018

Objectives : In present study, therefore, possible beneficial pharmacological activities of standard potato protein extracts (SPE) were observed on the mild diabetic obese mice. Methods : After end of 12 weeks of continuous oral administrations of three different dosages of SPE 400, 200 and 100 mg/kg, or metformin 250 mg/kg, analyzed the hepatoprotective, hypolipidemic, hypoglycemic, nephroprotective and anti-obesity effects, separately. In addition, liver antioxidant defense systems were additionally measured with lipid metabolism-related genes expressions and hepatic glucose-regulating enzyme activities for action mechanism. Results : All of diabetes and related complications including obesity were significantly inhibited by treatment of SPE 400, 200 and 100 mg/kg, dose-dependently, and they also dramatically normalized the hepatic lipid peroxidation and depletion of liver endogenous antioxidant defense system, the changes of the hepatic glucose-regulating enzyme activities, also changes of the lipid metabolism-related genes expressions including hepatic $AMPK{\alpha}1$ and $AMPK{\alpha}2$ mRNA expressions, dose-dependently. Especially, SPE 200 mg/kg constantly showed favorable inhibitory activities against type II diabetes and related complications as comparable to those of metformin 250 mg/kg in HFD mice, respectively. Conclusions : The present work demonstrated that SPE 400, 200 and 100 mg/kg showed favorable anti-diabetic and related complications including obesity refinement activities in HFD mice, through AMPK upregulation mediated hepatic glucose enzyme activity and lipid metabolism-related genes expression, antioxidant defense system and pancreatic lipid digestion enzyme modulatory activities.

• Journal of Nutrition and Health
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• v.56 no.6
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• pp.589-601
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• 2023

Purpose: Baicalein, a natural flavone found in herbs, exhibits diverse biological activities. Nonalcoholic steatohepatitis (NASH) is an irreversible condition often associated with a poor prognosis. This study aimed to evaluate the effects of baicalein on the development of NASH in mice. Methods: Male C57BL/6J mice were randomly divided into four groups. Three groups were fed a methionine-choline-deficient (MCD) diet to induce NASH and were simultaneously treated with baicalein (at doses of 50 and 100 mg/kg) or vehicle only (sodium carboxymethylcellulose) through oral gavage for 4 weeks. The control group was fed a methionine-choline-sufficient (MCS) diet without the administration of baicalein. Results: The baicalein treatment significantly reduced serum levels of alanine aminotransferase and aspartate aminotransferase, suggestive of reduced liver damage. Histological analysis revealed a marked decrease in nonalcoholic fatty liver activity scores induced by the MCD diet in the mice. Similarly, baicalein treatment at both doses significantly attenuated the degree of hepatic fibrosis, as examined by Sirius red staining, and hepatocellular death, as examined by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Baicalein treatment attenuated MCD-diet-induced lipid peroxidation, as evidenced by lower levels of hepatic malondialdehyde and 4-hydroxynonenal, demonstrating a reduction in oxidative stress resulting from lipid peroxidation. Moreover, baicalein treatment suppressed hepatic protein levels of 12-lipoxygenase (12-Lox) induced by the MCD diet. In contrast, baicalein enhanced the activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. Additionally, baicalein treatment significantly reduced hepatic non-heme iron concentrations and hepatic ferritin protein levels in mice fed an MCD diet. Conclusion: To summarize, baicalein treatment suppresses hepatic lipid peroxidation, 12-Lox expression, and iron accumulation, all of which are associated with the attenuation of NASH progression.