• Journal of Korean Medicine for Obesity Research
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• v.21 no.2
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• pp.49-58
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• 2021

Objectives: The purpose of this study was to investigate the effect of white pan bread added with Kamut (Triticum turgidum spp.) on high fat diet (HFD)-induced obese C57BL/6 mice. Methods: The white pan bread or white pan bread with Kamut (BK) were administered for 8 weeks in HFD-induced obese C57BL/6 mice. To evaluate the effect and its mechanisms of BK on obese mice, we measured body weight change, serum lipid profiles, histopathological analysis, and protein expression of CCAAT/enhancer binding protein-α (C/EBPα) in the liver. Results: Administration of BK significantly decreased body weight in HFD-induced obese mice. In addition, BK-administered group significantly reduced serum total cholesterol, glucose, and high-density lipoprotein cholesterol levels compared with the HFD-induced control group. The HFD-induced mice had damaged liver tissue and increased the size of adipose tissue, but BK-administered group attenuated liver damage and decreased the size of adipocyte. Furthermore, administration of BK significantly down-regulated C/EBPα in the liver compared with HFD-fed mice. In particular, BK-administered group has higher inhibited body weight, serum lipid profiles, and C/EBPα expressions than white pan bread-administered group. Conclusions: This study demonstrated that administration of BK attenuated HFD-induced obesity by regulation of C/EBPα than consumption of white pan bread. Therefore, BK could be developed as a bread for prevention of obesity.

• 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.

• Korean Journal of Agricultural Science
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• v.51 no.2
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• pp.159-167
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• 2024

Herbal medicinal mushroom Cordyceps militaris has been traditionally used as tonic medicine for metabolic syndrome. Cordycepin, main extract of C. militaris, has been reported with immunomodulatory, anticancer, and hepatoprotective effects. This study was conducted to evaluate the potential hepatoprotective effect of cordycepin-enriched Cordyceps militaris, against high fat diet (HFD)-induced hepatic steatosis (HS) in male obese (ob/ob) mice. HFD was provided to ob/ob mice ad libitum (except negative control). Cordycepin-enriched C. militaris extract powder (CM) was orally administered once daily at dose levels of 0, 125, 250, and 500 mg·kg^-1 for 4 weeks. During the study, body weight gain was statistically increased in all HFD fed groups compared to negative control, but body weight gain in CM 500 mg·kg^-1 treated group shows a low tendency compared to HS model group. In organ weights, absolute and relative weights (to body weight) in liver and perirenal adipose tissue were increased in all HFD treated groups except CM 500 mg·kg^-1 treated group compared to the negative control. In clinical chemistry, serum glucose and total cholesterol levels in CM 250 and/or 500 mg·kg^-1 treated groups were lower than HS model group. In microscopical examination, hepatocyte vacuolation with macrovesicles in HS model group was increased compared to negative control, but this finding was decreased in CM 500 mg·kg^-1 treated group compared to HS model group. In this study, CM exhibited hepatoprotective effects against hepatic steatosis at mg·kg^-1 in ob/ob mice.

• Journal of the East Asian Society of Dietary Life
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• v.15 no.4
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• pp.386-396
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• 2005

The effects of spirulina-added salad dressing on lipid profiles and antioxidant biomarkers such as total glutathionine, TBARS value, carbonyl value, GPx, GR, SOD and paraoxonase activity in plasma or liver of mice were evaluated Sixteen male ICR mice weighing 20$\pm$2 g were divided into two groups and fed low fat ($5\%$ fat) diet (low fat control: LFC) and low fat control plus dressing diet (LFD) for eight weeks. Body weight, tissue weights of liver, heart and kidney, and the distribution of body fat deposition were not significantly different between two groups. Also, the profile of TG, TC, LDL and HDL cholesterol were similar between two groups. The DNA damage was determined using the comet assay (single cell gel assay) with alkaline electrophoresis and quantified by measuring tail length (TL). Spirulina salad dressing consumption resulted in significant decrease in lymphocyte DNA damage expressed by TL (LFC: $28.8{\mu}m$, LFD: $20.3{\mu}m$). Additionally, salad dressing consumption for 8 wks decreased the lipid peroxidation assayed by TBARS to $12.6\%$ compared with the control. The levels of antioxidant vitamins such as $\beta$-carotene were significantly higher in plasma of LFD group than those in LFC group based on HPLC method This study shows that spirulina-added salad dressing exerts degenerative disease-protective effects on oxidative DNA damage and lipid peroxidation possibly via a free radical levels.

• Journal of Ginseng Research
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• v.43 no.2
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• pp.196-208
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• 2019

Background: Nonalcoholic steatohepatitis (NASH) is one of the chronic inflammatory liver diseases and a leading cause of advanced liver fibrosis, cirrhosis, and hepatocellular carcinoma. The main purpose of this study was to clarify the effects of GBCK25 fermented by Saccharomyces servazzii GB-07 and pectinase, on NASH severity in mice. Methods: Six-wk-old male mice were fed either a normal diet (ND) or a Western diet (WD) for 12 wks to induce NASH. Each group was orally administered with vehicle or GBCK25 once daily at a dose of 10 mg/kg, 20 mg/kg, 100 mg/kg, 200 mg/kg, or 400 mg/kg during that time. The effects of GBCK25 on cellular damage and inflammation were determined by in vitro experiments. Results: Histopathologic analysis and hepatic/serum biochemical levels revealed that WD-fed mice showed severe steatosis and liver injury compared to ND-fed mice. Such lesions were significantly decreased in the livers of WD-fed mice with GBCK25 administration. Consistently, mRNA expression levels of NASH-related inflammatory-, fibrogenic-, and lipid metabolism-related genes were decreased in the livers of WD-fed mice administered with GBCK25 compared to WD-fed mice. Western blot analysis revealed decreased protein levels of cytochrome P450 2E1 (CYP2E1) with concomitantly reduced activation of c-Jun N-terminal kinase (JNK) in the livers of WD-fed mice administered with GBCK25. Also, decreased cellular damage and inflammation were observed in alpha mouse liver 12 (AML12) cells and RAW264.7 cells, respectively. Conclusion: Administration of GBCK25 ameliorates NASH severity through the modulation of CYP2E1 and its associated JNK-mediated cellular damage. GBCK25 could be a potentially effective prophylactic strategy to prevent metabolic diseases including NASH.

• Journal of Nutrition and Health
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• v.26 no.3
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• pp.286-298
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• 1993

In order to investigate the effect of selenium (Se) on the liver damage, metallothionein synthesis and hepatic antioxidative detoxification system in cadmium(Cd) administered rats. Sprague-Dawley male rats(60\\5g) were divided into two diet groups, depending on with (CdS groups) or without (Cd groups) 0.5ppm Se supplementation and fed experimental diets ad libidum for 4 weeks. And then each group was again subdivided into five groups, depending on injection number of Cd, i.e., 0, 1, 2, 3, and 4 times of 2.5mg Cd/kg of body wt once a day. Hemoglobin concentration, hematocrit values, superoxide dismutase, glutathione peroxidase and glutathione S-transferase activite were decreased progressively with increasing number of Cd injection, but increased by the supplementation of Se. The reduced form of glutathione (GSH) contents in blood and liver and vitamin E content were decreased and oxidized form (GSSG) increased in Cd groups, but these of Se supplemented groups were not very different from controls. Cd reduced liver vitamin E content which was not restored by Se supplementation. Liver lipid peroxide values were elevated with increasing doses of Cd, but Se supplementation reduced these elevated levels. Accumulation of metallothionein in liver and kidney was increased with increasing number of Cd injection, but Se did not affect on them. Histological examination revealed that lysosomes were significantly increased and mitochondria and Golgi apparatus were enlarged by Cd, however, these changes were reduced by Se. It was concluded that Se administration promoted antioxidative detoxification and alleviated peroxidative damage in rat liver by Cd.

• Journal of Nutrition and Health
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• v.27 no.10
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• pp.1007-1017
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• 1994

In order to investigate the effect of Korean green tea, oolong tea and black tea beverage on the antioxidative detoxification in cadmium(Cd) poisoned rat liver, male Sprague-Dawley rat weighing 143$\pm$3.2g were divided into control and experimental groups. The experimental groups were fed standard diet containing 40ppm Cd and were given distilled water(CD), 5% black tea(BT), oolong tea(OT) and green tea(GT), respectively. Tea beverages were extracted from 5G dry leaves of teas in 100ml hot distilled water by the treatment at 85$^{\circ}C$ for 3 min. Liver xanthine oxidase(XOD) activity was increased by the administration of Cd except GT group. Liver superoxide dismutase(SOD), glutathione peroxidase(GSH-px), glutathione S-transferase(GST) activities were decreased by te administration of Cd but did not decreased by the administration of green tea(in GT group). Vitamin E and reduced glutathione contents were significantly decreased in Cd administered groups. Liver lipid peroxide value in Cd administered groups were increased compared to control group, but was not increased in GT group. Serum glutamic oxaloacetic transaminase(GOT) activities in CD, OT, BT groups were higher than control, but that in GT group was similar to control group. Serum glutamic pyruvic transaminase(GPT) activity was not significantly different among various groups. It was concluded that green tea might alleviate peroxidative damage in Cd-administered rat liver by reinforcing antioxidative detoxification system.

• Biomolecules & Therapeutics
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• v.22 no.5
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• pp.420-425
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• 2014

Esophageal reflux of gastric contents causes esophageal mucosal damage and inflammation. Recent studies show that oxygen-derived free radicals mediate mucosal damage in reflux esophagitis (RE). Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is one of the most abundant polyphenols in the human diet and possesses anti-inflammatory, antibacterial and anti-oxidant activities. In this context, we investigated the effects of CGA against experimental RE in rats. RE was produced by ligating the transitional region between the forestomach and the glandular portion and covering the duodenum near the pylorus ring with a small piece of catheter. CGA (10, 30 and 100 mg/kg) and omeprazole (positive control, 10 mg/kg) were administered orally 48 h after the RE operation for 12 days. CGA reduced the severity of esophageal lesions, and this beneficial effect was confirmed by histopathological observations. CGA reduced esophageal lipid peroxidation and increased the reduced glutathione/oxidized glutathione ratio. CGA attenuated increases in the serum level of tumor necrosis factor-${\alpha}$, and expressions of inducible nitric oxide synthase and cyclooxygenase-2 protein. CGA alleviates RE-induced mucosal injury, and this protection is associated with reduced oxidative stress and the anti-inflammatory properties of CGA.

• Herbal Formula Science
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• v.28 no.2
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• pp.179-187
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• 2020

Objectives : This study investigated the hepatoprotective effects effects of Jageum-jung extract on alcohol-induced liver disease mice model. Methods : Alcoholic liver disease was induced by Ethanol in C57/BL6 male mice, which were fed Lieber-DeCarli liquid diet containing ethanol. Jageum-jung (100,200 and 300 mg/kg bw/day) were orally administered daily in the alcoholic fatty liver disease mice for 16 days. Results : The results indicate that Jageum-jung promotes hepatoprotective effects by significantly reducing aspartate transaminase (AST) and alanine transaminase (ALT) levels as indicators of liver damage in the serum. Furthermore, Jageum-jung decreased accumulation of triglyceride and total cholesterol, increased levels of superoxide dismutase (SOD) and glutathione (GSH) in the serum of the alcoholic fatty liver disease mice model. Additionally, it improved the serum alcohol dehydrogenase (ADH) activity. Conclusions : This study confirmed the anti-oxidative and hangover elimination effects of Jageum-jung extract, and suggests the possibility of using Jageum-jung to treat alcholic liver disease.

• Journal of Haehwa Medicine
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• v.8 no.1
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• pp.425-449
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• 1999

For the evaluation of the effect on SWS, experiments were made on hyperlipidemia induced by hypercholesterol diet, inhibitory reaction to human platelet aggregation, Pulmonary thrombosis induced by collagen and epinephrine, global cerebral ischemia induced by KCN, brain ischemia induced by MCA occlusion, cytotoxicity of PC12 cells induced by amyloid ${\beta}$ protein(25-35), and NO production in RAW cells stimulated by lipopolysaccharide. The results were obtained as follows : 1. In the experiment on hyperlipidemia, the level of serum total cholesterol, phospholipid, and LDL-cholesterol were significantly decreased while the level of triglyceride, VLDL-cholesterol, and HDL-cholesterol had no significant change. 2. In the experiment on inhibitory reaction to platelet aggregation, SWS inhibited platelet aggregation induced by ADP(36.05%), by collagen(20.4%), and by thrombin(0.6%). 3. In the experiment on pulmonary thrombosis induced by collagen and epinephrine, the protective effect was found(37%). 4. In the experiment on global cerebral ischemia, coma duration induced by KCN changed insignificantly. 5. In the experiment on MCA occlusion, the change of neurologic grades on hind limb was significant only after the operation. Besides brain ischemic area and edema ratio were significantly decreased. 6. In the experiment on cytotoxicity of PC 12 cells induced by amyloid ${\beta}$ protein, the significant protective effect was found as concentration increases. 7. In the experiment on NO production in RAW cells stimulated by lipopolysaccharide, NO was significantly decreased. According to the results, it is expected that SWS might be effective on hyperlipidemia and brain damage.