• Nutrition Research and Practice
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• v.14 no.4
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• pp.334-351
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• 2020

BACKGROUND/OBJECTIVES: This study was designed to investigate the improvement effect of white ginseng extract (GS-KG9) on D-galactosamine (Ga1N)-induced oxidative stress and liver injury. SUBJECTS/METHODS: Sixty Sprague-Dawley rats were divided into 6 groups. Rats were orally administrated with GS-KG9 (300, 500, or 700 mg/kg) or silymarin (25 mg/kg) for 2 weeks. The rats of the GS-KG9- and silymarin-treated groups and a control group were then intraperitoneally injected Ga1N at a concentration of 650 mg/kg for 4 days. To investigate the protective effect of GS-KG9 against GalN-induced liver injury, blood liver function indicators, anti-oxidative stress indicators, and histopathological features were analyzed. RESULTS: Serum biochemical analysis indicated that GS-KG9 ameliorated the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in GalN-treated rats. The hepatoprotective effects of GS-KG9 involved enhancing components of the hepatic antioxidant defense system, including glutathione, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT). In addition, GS-KG9 treatment inhibited reactive oxygen species (ROS) production induced by GalN treatment in hepatocytes and significantly increased the expression levels of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) proteins, which are antioxidant proteins. In particular, by histological analyses bases on hematoxylin and eosin, Masson's trichrome, α-smooth muscle actin, and transforming growth factor-β1 staining, we determined that the administration of 500 mg/kg GS-KG9 inhibited hepatic inflammation and fibrosis due to the excessive accumulation of collagen. CONCLUSIONS: These findings demonstrate that GS-KG9 improves GalN-induced liver inflammation, necrosis, and fibrosis by attenuating oxidative stress. Therefore, GS-KG9 may be considered a useful candidate in the development of a natural preventive agent against liver injury.

• Nutrition Research and Practice
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• v.14 no.3
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• pp.175-187
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• 2020

BACKGROUND/OBJECTIVES: In this study, we investigated the beneficial effects of skate cartilage extracts containing chondroitin sulfate (SCS) on hyperlipidemia-induced inflammation and oxidative stress in high cholesterol diet (HCD)-fed mice in comparison with the effects of shark cartilage-derived chondroitin sulfate (CS). MATERIALS/METHODS: Low-density lipoprotein receptor knockout (LDLR-KO) mice were fed HCD with an oral administration of CS (50 and 100 mg/kg BW/day), SCS (100 and 200 mg/kg BW/day), or water, respectively, for ten weeks. RESULTS: The administration of CS or SCS reduced the levels of serum triglyceride (TG), total cholesterol (TC), and LDL cholesterol and elevated the levels of high-density lipoprotein cholesterol, compared with those of the control group (P < 0.05). Furthermore, CS or SCS significantly attenuated inflammation by reducing the serum levels of interleukin (IL)-1β and hepatic protein expression levels of nuclear factor kappa B, inducible nitric oxide synthase, cyclooxygenase-2, and IL-1beta (P < 0.05). In particular, the serum level of tumor necrosis factor-alpha was reduced only in the 100 mg/kg BW/day of SCS-fed group, whereas the IL-6 level was reduced in the 100 and 200 mg/kg BW/day of SCS-fed groups (P < 0.05). In addition, lipid peroxidation and nitric oxide production were attenuated in the livers of the CS and SCS groups mediated by the upregulation of hepatic proteins of antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase (P < 0.05). CONCLUSIONS: These results suggest that the biological effects of SCS, similar to those of CS, are attributed to improved lipid profiles as well as suppressed inflammation and oxidative stress induced by the intake of HCD.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.1
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• pp.19-26
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• 1993

In this study rats in fasting or fed protein free restricted diet including only fat showed much lowered level of serum cholesterol and triglyceride accompanied by utmost weight loss and high level of blood urea nitrogen indicated the tissue degradation, especially in liver with signs of damage or necrosis of hepatic parenchymal cell leading to elevated glutamic pyruvate transaminase value and to death. Rats fed only perilla oil in starvation or as fat source in normal diet dropped down the level of serum cholesterol and triglyceride compared to beef tallow fed rat. But with evidence of glutamic pyruvate transaminase values which was significantly elevated long term ingestion of perilla oil is likely to cause the lesion or any damage of hepatic function.

• Journal of Life Science
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• v.18 no.11
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• pp.1551-1560
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• 2008

Cytokines play a pivotal role in systemic inflammatory response following cardiac surgery with cardiopulmonary bypass (CPB). The purpose of this study was to investigate the perioperative changes in proinflammatory [tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin-6 (IL-6)] and antiinflammatory cytokines [interleukin-10 (IL-10)], and each correlation between the cytokines and other variables in valvular heart surgery with CPB. Serum IL-6 and IL-10 levels and leukocyte counts significantly increased following CPB. CPB caused hepatic, renal and myocardial dysfunctions. IL-6 levels had positive correlations with IL-10 levels at postoperative periods. TNF-$\alpha$ levels had correlations with leukocyte counts and myocardial marker levels at postoperative 24 hr (PO-24 h). Furthermore, IL-6 or IL-10 levels had positive correlations with other variable such as hepatic, renal or myocardial marker at postoperative periods. These results showed that balance between proinflammatory and antiinflammatory cytokines is maintained during cardiac surgery with CPB, and that these cytokines exert postoperatively inflammatory and antiinflammatory reactions.

• Journal of Life Science
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• v.19 no.10
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• pp.1360-1367
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• 2009

Liver fibrosis is a process of healing and scarring in response to chronic liver injury. Following injury, an acute inflammation response takes place resulting in moderate cell necrosis and extracellular matrix damage. To develop a novel therapeutic approach in hepatic fibrogenesis, we examined the simultaneous suppression of the transcription factors NF-$\kappa$B and Sp1, which regulate acute inflammation and continuous deposition of extracellular matrix in liver fibrosis. We employed chimeric decoy oligodeoxynucleotide containing the consensus sequences of both NF-$\kappa$B and Sp1 binding sites, to suppress these transcription factors simultaneously. Treatment of chimeric decoy oligodeoxynucleotide reduced the activity of hepatic stellate cells in vitro, and decreased the expression of fibrotic and proinflammatory gene responses in a mouse model of liver fibrosis. These results suggest that chimeric decoy oligodeoxynucleotide strategy can be a potential therapeutic application to prevent liver fibrosis.

• Biomolecules & Therapeutics
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• v.15 no.4
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• pp.252-260
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• 2007

As it is needed to assay possible feasibility of extrapolation between in vivo and in vitro systems and to develop a new in vitro method for toxicity testing, we investigated global gene expression from both animal and cell line treated with thioacetamide (TAA) and compared between in vivo and in vitro genomic profiles. For in vivo study, mice were orally treated with TAA and sacrificed at 6 and 24 h. For in vitro study, TAA was administered to a mouse hepatic cell line, BNL CL.2 and sampling was carried out at 6 and 24 h. Hepatotoxicity was assessed by analyzing hepatic enzymes and histopathological examination (in vivo) or lactate dehydrogenase (LDH) assay and morphological examination (in vitro). Global gene expression was assessed using microarray. In high dose TAA-treated group, there was centrilobular necrosis (in vivo) and cellular toxicity with an elevation of LDH (in vitro) at 24 h. Statistical analysis of global gene expression identified that there were similar numbers of altered genes found between in vivo and in vitro at each time points. Pathway analysis identified several common pathways existed between in vivo and in vitro system such as glutathione metabolism, bile acid biosynthesis, nitrogen metabolism, butanoate metabolism for hepatotoxicty caused by TAA. Our results suggest it may be feasible to develop toxicogenomics biomarkers by comparing in vivo and in vitro genomic profiles specific to TAA for application to prediction of liver toxicity.

• The Korean Journal of Food And Nutrition
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• v.23 no.1
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• pp.30-38
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• 2010

This study was conducted to determine the effects of vitamin C on the activity of liver function enzymes and electromicrographic changes in white rats treated with aflatoxin $B_1(AFB_1)$ or X-ray and $AFB_1$. Six week-old male Sprague-Dawley rats were randomly divided into five groups: a control group, $AFB_1$ treated group, $AFB_1$ treated group with vitamin C, X-ray and $AFB_1$ co-treated group, X-ray and $AFB_1$ co-treated group with vitamin C. On the first day of the experiment, only one dose of X-rays was exposed to the entire liver at 1,500 cGy. Next, vitamin C was injected at 10 mg/kg body weight by intraperitoneal injection, followed 1 hr later by the administration of 0.4 mg/kg of $AFB_1$ by intraperitoneal injection. These treatments were then administered every three days over a period of 15 days. On the 16th day of treatments, the animals were sacrificed. Analysis of the activity of the liver function enzymes, GOT, ALK phatase and LDH, in the sera of rats revealed that they were somewhat increased by $AFB_1$ treatment, X-ray and $AFB_1$ co-treatment when compared to the control group. Furthermore, the activity of these enzymes decreased in response to administration of vitamin C. Especially, the levels of GOT were remarkably decreased in the $AFB_1$ treated group treated with vitamin C when compared to the group treated with $AFB_1$ alone(p<0.001). Electromicrographic analysis revealed cloudy swelling, necrosis, vesicular degeneration and fat accumulation of hepatocytes in response to treatment with $AFB_1$ or co-treatment with X-ray and $AFB_1$. However, the destruction of hepatic cells was considerably lower in the vitamin C-treated group. These results indicate that vitamin C had ameliorating effects on the hepatic cell damage.

• 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.

• Applied Microscopy
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• v.39 no.4
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• pp.355-363
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• 2009

The purpose of this study was to demonstrate the effect of Momordica Charantia L. water extracts, one of the natural chelator, on the biochemical and enzyme activity changes in the rats liver and kidney caused by lead acetate. Rat approximately 250 g in weight were grouped into the control, lead acetate treated, and the Momordica Charantia L. boiling water extracts treated after lead acetate groups. Lead acetate (1,000 ppm) and Momordica Charantia L. water extracts (5%, 10%) were delivered drinking water. Serum AST, ALT and BUN were measured, histological alteration of liver and kidney were examined by light microscopy. Momordica Charantia L. extract group was decreased serum AST, ALT and BUN level induced by lead. Optical observations of liver tissue, lead group were observed necrosis of hepatic cells and infiltration of inflammatory cells, but Momordica Charantia L. extract group was observed only slight infiltration of inflammatory cells around the central vein. Optical observations of kidney tissue, lead acetate induced atrophy and necrosis of glomerulus and infiltration of inflammatory cell around renal tubule. For the group treated with Momordica charantia L. extract, the glomerulus was similar to the control, some around the renal tubule was observed infiltration of inflammatory cells. In conclusion, Momordica Charantia L. water extract may protect the lead-induced toxicity on liver and kidney.

• Journal of Life Science
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• v.18 no.10
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• pp.1342-1347
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• 2008

The purpose of present study was to investigate the protective effect of silkworm excrement powder (SEP) on alcohol-induced hepatotoxicity in rats. Semisynthetic diet supplemented with SEP (3%, w/w) given to alcohol-feeding rats for 30 days, then blood and tissues were collected, processed and used for alcohol concentration mensuration, various biochemical estimations and histopathological examination. Chronic alcohol administration resulted in significantly increase in the activities of the clinically important liver marker enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST), $\gamma$-glutamyl transpeptidase ($\gamma$-GTP) and lactate dehydrogenase (LDH). Also, a highly significant increase in the blood alcohol level by alcohol treatment was observed. But alcohol-induced elevation of ALT and LDH levels markedly prevented and the level of blood alcohol decreased in SEP treated rats as compared to alcohol-administered control rats. SEP supplementation showed highly decreased the concentrations of total lipid, triglyceride and cholesterol in serum, as compared with alcohol treated control rats. Alcohol treatment induced the marked accumulation of large lipid droplets, hepatocytes necrosis and inflammation in the liver, but SEP administration attenuated to alcohol-induced accumulation of lipid droplets and hepatocyte necrosis. The results indicated that SEP may exert a protective effect against alcoholic hepatotoxicity through decreasing the activity of hepatic marker enzymes.