• Proceedings of the PSK Conference
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• 2003.10b
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• pp.198.2-198.2
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• 2003

The anti-oxidant activities of fucosterol isolated from the marine algae Pelvetia siliquosa were investigated. Fucosterol exhibited a significant decrease in serum transaminase activities elevated by hepatic damage induced by CCl$_4$-intoxication in rats. Fucosterol inhibited the sGOT and sGPT activities by 25.57 and 63.16%, respectively. Fucosterol showed the increase in the anti-oxidant enzymes such as hepatic cytosolic superoxide dismutase, catalase and glutathione peroxidase activities by 33.89, 21.56 and 39.24%, respectively, in CCl$_4$-intoxicated rats. (omitted)

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.9
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• pp.1161-1166
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• 2009

The purpose of the present study was to effect of red pepper seeds powder on antioxidative defense system and oxidative damage in rats fed high fat high cholesterol diet. Rats were divided into five experimental groups which are composed of normal diet group, high fat high cholesterol diet group, high fat high cholesterol diet with 5% red pepper seeds powder supplemented group (SA group), high fat high cholesterol diet with 10% red pepper seeds powder supplemented group (SB group), and high fat.high cholesterol diet with 15% red pepper seeds powder supplemented group (SC group). Supplementation of red seed pepper groups (SA, SB, and SC groups) resulted in increased activities of hepatic glutathione peroxidase and superoxide dismutase. However, there was no significant difference in the activity of hepatic catalase among all experimental groups. Hepatic superoxide radical contents in microsome and mitochondria were significantly reduced in red pepper seeds powder supplemented groups. Hepatic hydrogen peroxide contents in mitochondria were significantly reduced 15% red pepper seeds powder supplemented group. Hepatic carbonyl values in microsome were significantly reduced in 10% and 15% red pepper seeds powder supplemented groups. Thiobarbituric acid reaction substance (TBARS) values in liver and plasma were reduced in red pepper seeds powder supplemented groups. These result suggest that red pepper seeds powder may reduce oxidative damage by the activation of antioxidative defense system in rats high fat.high cholesterol diets.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.10
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• pp.1271-1278
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• 2007

In this study, the ability of Styela clava or Styela plicata to reduce ethanol-induced hepatotoxicity and hepatic and leucocytic DNA damages was evaluated. Twenty four male SD rats were given 25% ethanol containing water (ad lib, p.o.) and divided into 3 groups; ethanol treated control group (EtOH), ethano1+3% S. clava (EtOH+SC), and ethano1+3% S. plicata (EtOH+SP). After 6 weeks, the supplementation of S. clava reduced the plasma ALT, ALP and LDH activities significantly (p<0.05), while S. plicata induced significant decrease in the plasma LDH activity only. The comet assay was employed to quantify the alcohol-induced DNA damage in rat hepatocytes and leucocytes. A significant protective effect on hepatic and leucocytic DNA damages was observed in S. clava or S. plicata supplemented groups compared to the EtOH control group. The hepatic DNA damage was correlated positively with plasma ALP and LDH activities. These results demonstrated that S. clava or S. plicata supplementation protected alcohol-induced hepatic and leucocytic DNA damage.

• Journal of Trauma and Injury
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• v.28 no.3
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• pp.211-214
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• 2015

The primary and secondary survey was designed to identify all of a patient's injuries and prioritize their management. However 15 to 22.3% of patient with missed injuries had clinically significant missed injuries. To reduce missed injury, special attention should be focused on patients with severe anatomical injury or obtunded. Victims of blunt trauma commonly had multiple system involvement. Some reports indicate that inexperience, breakdown of estalished protocol, clinical error, and restriction of imaging studies may be responsible for presence of missed injury. The best way of reducing clinical significant of missed injuries was repeated clinical assessment. Here we report a case of severe blunt hepatic injury patient and pericardial injury that was missed in primary and secondary survey. After damage control surgery of hepatic injury, she remained hemodynamically unstable. Further investigation found cardiac tamponade during intensive care. This was managed by pericardial window operation through previous abdominal incision and abdominal wound closure was performed.

• Nutrition Research and Practice
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• v.4 no.1
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• pp.11-15
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• 2010

The purpose of the present study was to investigate the effect of ethanol extracts from red pepper seeds on the antioxidative defense system and oxidative stress in rats fed a high fat high cholesterol diet. Rats were divided into four experimental groups which were composed of high fat high cholesterol diet group (HF), high fat high cholesterol diet with 0.1% ethanol extracts from red pepper seeds supplemented group (HEA), high fat high cholesterol diet with 0.2% ethanol extracts from red pepper seeds supplemented group (HEB) and high fat high cholesterol diet with 0.5% ethanol extracts from red pepper seeds supplemented group (HEC). Supplementation of ethanol extracts from red pepper seeds groups (HEA, HEB and HEC) resulted in significantly increased activities of hepatic glutathione peroxidase and catalase. Hepatic superoxide radical contents in microsome and mitochondria were significantly reduced in the groups supplemented with red pepper seeds ethanol extracts. Hepatic hydrogen peroxide content in the mitochondria was reduced in ethanol extracts from red pepper seeds supplemented groups. TBARS values in the liver were reduced in red pepper seeds ethanol extracts supplemented groups. Especially, HEB and HEC groups were significantly decreased compared to the HF group. Hepatic carbonyl values were significantly reduced in mitochondria in these supplemented groups. These results suggest that red pepper seeds ethanol extracts may reduce oxidative damage, by activation of antioxidative defense system in rats fed high fat high cholesterol diets.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.1
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• pp.15-18
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• 1993

To evaluate an effect of dietary protein on the intoxication of methanethiol in rats, the methanethiol was intraperitoneally injected to the rats fed a low or high protein diet and then the liver weight per body weight and seurm levels of alanine aminotransferase (ALT) activities were determined to investigate the differences in liver damage between the animal groups fed low protein diet and that fed high protein diet. On the other hand, the hepatic glutathione content and its conjugating enzyme, glutathione S-transferase (GST) activity were determined to clarify the cause of difference in liver function between the two groups. The increasing rate of liver weigh/body wt., serum levels of ALT to its control group were higher in methanethiol-treated rats fed low protein diet than those fed high protein diet. The hepatic content of glutathione and GST activity were higher in rats fed high protein diet than those fed low protein diet and the decreasing rate of hepatic glu-tathione content to its control group was higher in rats fed low protein diet than those fed high protein diet. Furthermore, the hepatic GST activity in methanethiol-treated rats was higher in rats fed high protein diet than those fed low protein diet. In case of control group, the GST activity was also higher in rats fed high protein diet than those fed low protein diet.

• BMB Reports
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• v.40 no.6
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• pp.1039-1049
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• 2007

Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.

• IMMUNE NETWORK
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• v.15 no.3
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• pp.125-134
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• 2015

Acute graft-versus-host-disease (GVHD) is characterized by selective damage to the liver, the skin, and the gastrointestinal tract. Following allogeneic hematopoietic stem cell transplantation, donor bone marrow (BM) cells repopulate the immune system of the recipient. We previously demonstrated that the acute intestinal GVHD (iGVHD) mortality rate was higher in MyD88-deficient BM recipients than that in the control BM recipients. In the present study, the role of MyD88 (expressed by donor BM) in the pathophysiology of hepatic GVHD (hGVHD) was examined. Unlike iGVHD, transplantation with MyD88-deficient T-cell depleted (TCD) BM attenuated hGVHD severity and was associated with low infiltration of T cells into the liver of the recipients. Moreover, GVHD hosts, transplanted with MyD88-deficient TCD BM, exhibited markedly reduced expansion of $CD11b^+Gr-1^+$ myeloidderived suppressor cells (MDSC) in the liver. Adoptive injection of the MDSC from wild type mice, but not MyD88-deficient mice, enhanced hepatic T cell infiltration in the MyD88-deficient TCD BM recipients. Pre-treatment of BM donors with LPS increased MDSC levels in the liver of allogeneic wild type BM recipients. In conclusion, hGVHD and iGVHD may occur through various mechanisms based on the presence of MyD88 in the non-T cell compartment of the allograft.

• Journal of Microbiology and Biotechnology
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• v.23 no.3
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• pp.405-413
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• 2013

Monocyte chemotactic protein-3 (MCP-3), a chemokine that is in a superfamily of structurally related small chemotactic cytokines involved in leukocyte trafficking, is regarded as a key factor in atherogenesis. In this study, we examined the changes in atherogenic parameters including hepatic lipid accumulation and oxidative balance in MCP- 3-overexpressing transgenic mice (MCP-3 mice) under atherogenic conditions. To induce an extreme atherogenic condition, mice were fed a high-fat, high-cholesterol (HFHC) diet for 12 weeks. The body weight and food intake were not changed by MCP-3 overexpression in the aorta. On a HFHC diet, the MCP-3 mice had higher plasma levels of total cholesterol and a higher atherogenic index compared with wild-type mice, although there were no differences in the plasma HDL-cholesterol and triglyceride levels. Furthermore, an increase in lipid accumulation was observed in the aortas as well as the livers of the HFHC diet-fed MCP-3 mice compared with wild-type mice. The activities of antioxidant enzymes increased in the livers of the HFHC diet-fed MCP-3 mice, whereas supplementation with antioxidants, naringin and hesperidin, reversed the activities of the hepatic antioxidant enzymes in HFHC diet-fed MCP-3 mice, indicating that there might be more oxidative damage to the tissues in the HFHC diet-fed MCP-3 mice leading to progression towards atherosclerosis and hepatic steatosis. Microarray analyses of the aorta revealed atherosclerosis-, PPARs-, lipoprotein receptor, and apolipoprotein-related genes that were affected by the HFHC diet in MCP-3 mice. These findings suggest that aortic MCP-3 overexpression may contribute to the development of atherosclerosis and hepatic steatosis under atherogenic conditions.

• Journal of Ginseng Research
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• v.41 no.3
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• pp.316-325
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• 2017

Background: Ginseng essence (GE) is a formulation comprising four medicinal and edible herbs including ginseng (Panax ginseng), American ginseng (Panax quinquefolius), lotus seed (Nelumbo nucifera), and lily bulb (Lilium longiflorum). This study was aimed at investigating the hepatoprotective effect of GE against carbon tetrachloride ($CCl_4$)-induced liver injury in rats. Methods: We treated Wistar rats daily with low, medium, and high [0.625 g/kg body weight (bw), 1.25 g/kg bw, and 3.125 g/kg bw, respectively] doses of GE for 9 wk. After the 1st wk of treatment, rats were administered 20% $CCl_4$ (1.5 mL/kg bw) two times a week to induce liver damage until the treatment ended. Results: Serum biochemical analysis indicated that GE ameliorated the elevation of aspartate aminotransferase and alanine aminotransferase and albumin decline in $CCl_4$-treated rats. Moreover, $CCl_4$-induced accumulation of hepatic total cholesterol and triglyceride was inhibited. The hepatoprotective effects of GE involved enhancing the hepatic antioxidant defense system including glutathione, glutathione peroxidase, glutathione reductase, glutathione S-transferase, superoxide dismutase, and catalase. In addition, histological analysis using hematoxylin and eosin and Masson's trichrome staining showed that GE inhibited $CCl_4$-induced hepatic inflammation and fibrosis. Furthermore, immunohistochemical staining of alpha-smooth muscle actin indicated that $CCl_4$-triggered activation of hepatic stellate cells was reduced. Conclusion: These findings demonstrate that GE improves $CCl_4$-induced liver inflammation and fibrosis by attenuating oxidative stress. Therefore, GE could be a promising hepatoprotective herbal formulation for future development of phytotherapy.