• Korean Journal of Food Science and Technology
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• v.37 no.4
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• pp.624-630
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• 2005

Glycoprotein (60 kDa) isolated from Ficus Carica Linnoeus (FCL glycoprotein) was examined by evaluating its hypolipidemic effects on plasma cholesterol levels and hepatic detoxicant enzyme activities in ICR mice. FCL glycoprotein $(100{\mu}g/mL)$ had strong scavenging activities (38%) against lipid peroxyl radicals. When mice were treated with Triton WR-1339 (400 mg/kg), levels of total cholesterol (TC) and low-density lipoprotein (LDL)-cholesterol in plasma significantly increased by 53.9 and 47.5 mg/dL, respectively, compared to the control, whereas, when pretreated with FCL glycoprotein $(100{\mu}g/mL)$, decreased remarkably by 55.4, and 47,0 mg/dL, compared to Triton WR-1339 treatment alone. Interestingly, high-density lipoprotein (HDL)-cholesterol level did not change. Body and liver weights did not change significantly after Triton WR-1339 treatment in presence of FCL glycoprotein. FCL glycoprotein $(100{\mu}g/mL)$ stimulated activities of antioxidative detoxicant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), whereas GPx activity significantly increased compared to the control. These results suggest FCL glycoprotein has abilities to scavenge lipid peroxyl radicals, lower plasma lipid levels, and stimulate detoxicant enzyme activity in mouse liver.

• Journal of the Korean Society of Food Science and Nutrition
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• v.39 no.2
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• pp.227-236
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• 2010

This study was carried out to investigate the anti-oxidative and anti-inflammatory actions of Hericium erinaceus mycelia in BALB/C mice injected with lopopolysaccharide (LPS), called endotoxin. Mice (6 weeks of age) weighing approximately $24.73\pm0.11$ g were divided into 5 groups and were fed on the experimental diets containing Hericium erinaceus mycelia powder (HMP) for 1 week. Experimental groups were NC (normal control), HMP-C (HMP control), LC (LPS control), HMP 3%, and HMP 10%. Endotoxin shock was induced by intraperitoneal injection of LPS (100 mg/kg BW). NC and HMP-C groups were injected with saline solution (100 mg/kg BW). Food efficiency ratio were significantly (p<0.05) decreased in the HMP supplementation groups. Total fat and $\beta$-glucan excretion were higher in HMP supplementation groups than NC and LC groups, while plasma TG level was not different among groups. Plasma ALT levels were significantly (p<0.05) lower in the HMP supplementation groups than in LC group at 8 hr after LPS injection, while tumor necrosis factor-$\alpha$ and interleukine-6 levels of plasma were not different among groups. Hepatic superoxide dismutase, glutathione-reductase (GSH-red), and glutathione-peroxidase activities were higher in the HMP supplementation groups than in LC group at 4 hr after intraperitoneal injection of LPS. Hepatic GSH levels and protein expression of GSH-red was significantly (p<0.05) higher in the HMP supplemented groups than in LC group at 1 hr, 4 hr and 8 hr after LPS injection. From the above results, it is concluded that Hericium erinaceus mycelia may ameliorate hepatic oxidative stress by LPS through the elevation of hepatic glutathione level and antioxidant enzyme activities, which support the hepatoprotective effect of Hericium erinaceus mycelia.

• Journal of the Korean Society of Food Science and Nutrition
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• v.21 no.5
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• pp.484-489
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• 1992

The present study was designed to evaluate the effects of dietary coenzyme $Q_{10}$ and vitamin E on hepatic lipid metabolism changes in adriamy cin(ADR)-treated rats. ADR treatment significantly increased the plasma levels of lipid peroxide in rats. But this increase was reduced by dietary supplementation of coenzyme $Q_{10}$ or vitamin E. Catalase and glutathione peroxidase activities were not greatly changed by ADR treatment, but the activities were significantly increased by dietary coenzyme $Q_{10}$. There was a tendency of lower superoxide dismutase activity in ADR-treated rats. However, coenzyme $Q_{10}$ administration induced this enzyme activity. The contents of cholesterol and phospholipid in liver were elevated by ADR-treated. Dietary coenzyme $Q_{10}$ reduced the increased hepatic cholesterol content in ADR-treated rat.

• BMB Reports
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• v.46 no.10
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• pp.513-518
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• 2013

We investigated the protective effects of Gymnaster koraiensis against oxidative stress-induced hepatic cell damage. We used two different cytotoxicity models, i.e., the administration of tert-butyl hydroperoxide (t-BHP) and acetaminophen, in HepG2 cells to evaluate the protective effects of G. koraiensis. The ethyl acetate (EA) fraction of G. koraiensis and its major compound, 3,5-di-O-caffeoylquinic acid (DCQA), exerted protective effects in the t-BHP-induced liver cytotoxicity model. The EA fraction and DCQA ameliorated t-BHP-induced reductions in GSH levels and exhibited free radical scavenging activity. The EA fraction and DCQA also significantly reduced t-BHP-induced DNA damage in HepG2 cells. Furthermore, the hexane fraction of G. koraiensis and its major compound, gymnasterkoreayne B (GKB), exerted strong hepatoprotection in the acetaminophen-induced cytotoxicity model. CYP 3A4 enzyme activity was strongly inhibited by the extract, hexane fraction, and GKB. The hexane fraction and GKB ameliorated acetaminophen-induced reductions in GSH levels and protected against cell death.

• Journal of Microbiology and Biotechnology
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• v.23 no.6
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• pp.785-793
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• 2013

We studied the effects of 2 different dosages of high-molecular-weight poly-${\gamma}$-glutamic acid (hm ${\gamma}$-PGA) derived from Bacillus subtilis chungkookjang on lipid metabolism in a high-fructose diet-induced hypertriglyceridemic animal model. For 4 weeks, rats were fed either AIN-93 diet (normal control, NC; n = 10) or modified AIN-93 diet in which cornstarch was substituted with 63% fructose (n = 30) to induce hypertriglyceridemia. After 4 weeks, the hypertriglyceridemic rats were treated with daily oral doses of 0 mg (hypertriglyceridemic control, HC), 2.5 mg (hypertriglyceridemic, low hm ${\gamma}$-PGA, HL), or 5 $mg{\cdot}kg{\cdot}bw^{-1}{\cdot}d^{-1}$ (hypertriglyceridemic, high hm ${\gamma}$-PGA, HH) hm ${\gamma}$-PGA for 4 weeks. The HL and HH groups exhibited significantly lower levels of serum triglyceride, total cholesterol, LDL cholesterol, and free fatty acids than the HC group. The administration of hm ${\gamma}$-PGA reduced serum ALT and AST levels. The activities of lipogenic enzymes such as hepatic malic enzyme and glucose-6-phosphate dehydrogenase as well as glucose-6-phosphate dehydrogenase mRNA expression were significantly decreased by hm ${\gamma}$-PGA administration (p < 0.05). These results indicate that hm ${\gamma}$-PGA has an anti-hypertriglyceridemic effect in high-fructose diet-induced hypertriglyceridemic rats.

• 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 Radiation Industry
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• v.7 no.1
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• pp.81-85
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• 2013

This study was conducted to investigate the effect of fermented blackberry drinks (BD) on carbon tetrachloride ($CCl_4$)-induced liver injury in rats. Male Sprague-Dawley rats were randomly divided into four groups with 6 rats per group: control, $CCl_4$, $CCl_4$ plus BD $3ml\;kg^{-1}$, and $CCl_4$ plus BD $6ml\;kg^{-1}$. We found that the levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were significantly increased and the activity of antioxidant enzyme glutathione peroxidase (GPx) in the liver was decreased in rats treated with $CCl_4$ alone when compared with the control group. However, the administration of BD attenuated the levels of serum AST and ALT in $CCl_4$-treated rats. Moreover, the administration of BD significantly increased the activity of GPx in $CCl_4$-treated rat livers. Taken together, these results suggest that BD could protect the liver from $CCl_4$-induced hepatic damage.

• Nutrition Research and Practice
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• v.13 no.5
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• pp.367-376
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• 2019

BACKGROUND/OBJECTIVE: The blue honeysuckle berry (Lonicera caerulea var. edulis L.) is a small deciduous shrub belonging to the Caprifoliaceae family that is native to Russia, China, Japan, and Korea. The berry of this shrub is edible, sweet and juicy and is commonly known as the blue honeyberry (BHB). This study examined the anti-diabetic potential of BHB on high-fat-diet-induced mild diabetic mice. The hypoglycemic, and nephroprotective effects of the 12-week oral administration of blue honeyberry extract were analyzed. MATERIALS/METHODS: The hypoglycemic effects were based on the observed changes in insulin, blood glucose, and glycated hemoglobin (HbA1c). Furthermore, the changes in the weight of the pancreas, including its histopathology and immunohistochemical investigation were also performed. Moreover, the nephroprotective effects were analyzed by observing the changes in kidney weight, its histopathology, blood urea nitrogen (BUN), and serum creatinine levels. RESULTS: The results showed that the high-fat diet (HFD)-induced control mice showed a noticeable increase in blood glucose, insulin, HbA1c, BUN, and creatinine levels. Furthermore, growth was observed in lipid droplet deposition related to the degenerative lesions in the vacuolated renal tubules with the evident enlargement and hyperplasia of the pancreatic islets. In addition, in the endocrine pancreas, there was an increase in the insulin-and glucagon-producing cells, as well as in the insulin/glucagon cell ratios. On the other hand, compared to the HFD-treated mice group, all these diabetic and related complications were ameliorated significantly in a dose-dependent manner after 84 days of the continuous oral administration of BHBe at 400, 200 and 100 mg/kg, and a dramatic resettlement in the hepatic glucose-regulating enzyme activities was observed. CONCLUSIONS: By assessing the key parameters for T2DM, the present study showed that the BHBe could act as a potential herbal agent to cure diabetes (type II) and associated ailments in HFD-induced mice.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.5
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• pp.611-616
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• 2013

Alcoholic liver disease (ALD) is a major cause of morbidity and mortality around the world. Although much progress has been made in understanding the pathogenesis of ALD, there remains no effective therapy for it. Accumulated evidence indicates that oxidative stress is the main pathological factors in the development of ALD. Ethanol administration causes accumulation of reactive oxygen species (ROS), including superoxide, hydroxyl radical, and hydrogen peroxide. ROS, in turn, cause lipid peroxidation of cellular membranes, and protein and DNA oxidation, which results in hepatocyte injury. In addition to pro-oxidants formation, antioxidants depletion caused by ethanol administration also results in oxidative stress. The objective of this study is to investigate the effects of Shiryung-tang extract on the chronic alcoholic liver injury induced by EtOH. Male Sprague Dawley rats were used in this study. All rats were maintained under standard laboratory conditions ($23{\pm}1^{\circ}C$, 12h light/12h dark cycles). All animals (n=30) were randomly divided into following groups: (1) Normal group, treated with distilled water (n=10); (2) Control group, treated with ethanol (n=10); (3) Sample group, treated with ethanol + pharmacopuncture (n=10). For oral administration of ethanol in Control and Sample group, the ethanol was dissolved in distilled water in concentrations of 25%(v/v). Throughout the experiment of 8 week, the rats were allowed free access to water and standard chow. Sample group were administrated by Shiryung-tang extract daily for 8 weeks. Control group were given normal saline for same weeks. As a results, the oral administration of ethanol for 8 weeks leads to hepatotoxicity. The levels of hepatic marker such as HDL-cholesterol, triglyceride, aspartate aminotransferase and alanine aminotransferase were altered. The ethanol also increased lipid peroxidation and depletion of antioxidant enzyme activities as well as hepatic tissue injury. However, the treatment of Shiryung-tang extract prevented all the alterations induced by ethanol and returned their levels to near normal. These data suggest that Shiryung-tang extract could have a beneficial effect in inhibiting the oxidative damage induced by chronic ethanol administration. Therefore, Shiryung-tang extract can be a candidate to protect against EtOH-induced liver injury.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.3
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• pp.276-283
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• 2007

This study was carried out to investigate the effect of isoflavone on the atherogenic effect in C57BL/6 mice. C57BL/6 female mice, 5 weeks of age, were fed on chow diets for 2 weeks during adjustment period. Mice weighing approximately $17.9{\pm}0.9\;g$ were divided into 4 groups and were fed on the experimental diets containing isoflavone for 8 weeks. Experimental groups were control (atherogenic diet), IF-10 (atherogenic diet with isoflavone 10 mg/100 g diet), IF-40 (atherogenic diet with isoflavone 40 mg/100 g diet) and IF-100 (atherogenic diet with isoflavone 100 mg/100 g diet). Food efficiency ratio was not different among the experimental groups. Plasma triglyceride (TG) concentrations were lower after 4 weeks in isoflavone supplementation groups than in control group, whereas monocyte chemoattractant protein-1 and thiobarbituric acid reactive substances (TBARS) levels of plasma were significantly (p<0.05) decreased in the isoflavone supplementation groups in a dose dependent manner. Both hepatic TG and cholesterol levels were significantly lowered in IF-100 than control. Hepatic glutathione concentrations were higher in the IF-100 group than in the other groups. Hepatic antioxidant enzyme activities including glutathione-reductase, glutathione-peroxidase, catalase, and Mn-superoxide dismutase were significantly higher in the isoflavone supplemen-tation groups in a dose dependent manner. From the above results, it is concluded that isoflavone may reduce the risk of atherosclerosis via hypolipidemic, anti-oxidative and anti-inflammatory effects.