• Nutrition Research and Practice
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• v.4 no.5
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• pp.369-374
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• 2010

Grape is one of the most popular and widely cultivated fruits in the world. Although grape skin and seeds are waste product of the winery and grape juice industry, these wastes contain large amounts of phytochemicals such as flavonoids, phenolic acids, and anthocyanidins, which play an important role as chemopreventive and anticancer agents. We evaluated efficacies of grape skin and seeds on hepatic injury induced by dimethylnitrosamine (DMN) in rats. Treatment with DMN significantly increased levels of serum alanine transaminase, aspartate transaminase, alkaline phosphatase, and bilirubin. Diet supplementation with grape skin or seeds (10% daily for 4 weeks) prevented these elevations. The grape skin and seeds also restored serum albumin and total protein levels, and reduced the hepatic level of hydroxyproline and malondialdehyde. Furthermore, grape skin and seeds reduced DMN-induced collagen accumulation, as estimated by histological analysis of liver tissue stained with Sirius red. Grape skin and seeds also reduced hepatic stellate cell activation, as assessed by ${\alpha}$-smooth muscle actin staining. In conclusion, grape skin and seeds exhibited in vivo hepatoprotective and antifibrogenic effects against DMN-induced liver injury, suggesting that grape skin and seeds may be useful in preventing the development of hepatic fibrosis.

• BMB Reports
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• v.46 no.12
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• pp.567-574
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• 2013

Liver plays a major role in maintaining glucose homeostasis in mammals. Under fasting conditions, hepatic glucose production is critical as a source of fuel to maintain the basic functions in other tissues, including skeletal muscle, red blood cells, and the brain. Fasting hormones glucagon and cortisol play major roles during the process, in part by activating the transcription of key enzyme genes in the gluconeogenesis such as phosphoenol pyruvate carboxykinase (PEPCK) and glucose 6 phosphatase catalytic subunit (G6Pase). Conversely, gluconeogenic transcription is repressed by pancreatic insulin under feeding conditions, which effectively inhibits transcriptional activator complexes by either promoting post-translational modifications or activating transcriptional inhibitors in the liver, resulting in the reduction of hepatic glucose output. The transcriptional regulatory machineries have been highlighted as targets for type 2 diabetes drugs to control glycemia, so understanding of the complex regulatory mechanisms for transcription circuits for hepatic gluconeogenesis is critical in the potential development of therapeutic tools for the treatment of this disease. In this review, the current understanding regarding the roles of two key transcriptional activators, CREB and FoxO1, in the regulation of hepatic gluconeogenic program is discussed.

• Biomolecules & Therapeutics
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• v.16 no.1
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• pp.34-39
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• 2008

Oxidative stress may represent a common link between chronic liver damage and hepatic fibrosis. In the present study, we investigated activity changes of sphingomyelin catabolic enzymes, such as sphingomyelinases and ceramidases by using dimethylnitrosamine (DMN)-treated Sprague-Dawley (SD) male rats hepatic fibrosis model as a hepatic fibrosis model. Twenty rats divided into five groups received: (1) saline; (2) DMN for 1 week, (3) DMN for 2 weeks, (4) DMN for 3 weeks, and (5) DMN for 4 weeks by intraperitoneally 10 mg/kg of body weight for three consecutive days a week. Activities of acidic and neutral sphingomyelinases and acidic, neutral and alkaline ceramidases were measured in the liver and kidney from DMN-treated rats. We found increased ceramidase activities from 2-week and/or 3-week DMN treated rat livers compared to control rat liver. Acidic sphingomyelinase and alkaline ceramidase activities were significantly increased in 3-week DMN-treated rat kidneys compared to control rat kidney. Therefore, sphingolipid metabolizing enzymes and sphingolipid metabolites are supposed to be involved in liver fibrosis, although further investigation is necessary to elucidate meanings of sphingolipids during the liver fibrosis

• Natural Product Sciences
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• v.17 no.3
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• pp.216-220
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• 2011

Activation of hepatic stellate cells (HSCs) characterized by increased proliferation and extracellular matrix deposition is identified as the major pathological feature of hepatic cirrhosis. Therefore, suppression of HSC activation has been proposed as an important antifibrotic therapeutic strategy. In the present study, we investigated the antiproliferative activity of root barks of Ulmus davidiana var. japonica (Ulmaceae) by employing HSC-T6 hepatic stellate cells as an in vitro assay system. Further investigation of the n-hexane and $CHCl_3$ fractions of root barks of U. davidiana var japonica led to the isolation of six triterpenoids: friedelin (1), epifridelanol (2), oleanolic acid (3), maslinic acid (4), ${\beta}$-amyrin (5) and ${\alpha}$-amyrin (6), together with ${\beta}$-sitosterol (7) and daucosterol (8). Among these compounds, 2, 3 and 4 significantly inhibited HSC proliferation. In addition, 4 inhibited HSC proliferation in time- and concentration-related manners, via a partially direct toxic effect, as assessed by morphological changes and release of lactate dehydrogenase.

• Journal of Trauma and Injury
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• v.29 no.2
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• pp.47-50
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• 2016

Transcatheter arterial embolization (TAE) for blunt hepatic injury in children is not common and is especially rare after damage control surgery (DCS). We report a successful TAE after DCS on a child for massive bleeding from the left hepatic artery due to a motor vehicle accident. The car (a sport utility vehicle) ran over the chest and abdomen of a 4-year-old boy. On arrival, initial vital signs were as follows: blood pressure, 70/40 mmHg; heart rate, 149/min; temperature, $36.7^{\circ}C$; respiratory rate, 38/min. After resuscitation, computed tomography was done, and a suspicious contrast leakage from a branch of the left hepatic artery and a spleen injury (grade V) were found. TAE was performed successfully after DCS for a liver injury.

• Herbal Formula Science
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• v.18 no.2
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• pp.259-265
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• 2010

Objectives : The purpose of this study is to report the improvement after Sweet BV herbal acupuncture therapy of shoulder impingement syndrome with Subacromial bursitis. Methods : We treated a patient having shoulder pain due to shoulder impingement syndrome with Sweet BV herbal acupuncture therapy. We checked visual analogue scale (VAS) score and range of movement (ROM). Results : We treated shoulder pain. Thereafter ROM improved and VAS score dropped to the level 3 points from 10 points at onset. Conclusions : This report shows Sweet BV herbal acupuncture therapy has effectiveness on shoulder impingement syndrome with Subacromial bursitis.

• YAKHAK HOEJI
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• v.40 no.1
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• pp.78-83
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• 1996

An ethanol administration causes hepatic triglyceride accumulation in rats. To assess whether the herbal extract containing Phaseoli radiati semen(herbal extract) inhibit s the triglyceride accumulation in the liver, we determined the hepatic triglyceiide levels in rats fed ethanol and the herbal extract. In addition, the blood ethanol concentrations and the activities of hepatic alcohol dehydrogenase(ADH) and aldehyde dehydrogenase(ALDH) were measured to determine the effects of the herbal extract on alcohol metabolism in rats. The administration of the herbal extract markedly reduced the triglyceride levels elevated by ethanol in the liver as well as in the serum. The herbal extract remarkably lowered blood ethanol concentrations in a dose-dependent manner. The ADH activities decreased by ethanol were recovered to the normal level by the herbal extract treatment. Moreover, the ALDH activities slightly decreased by ethanol increased beyond the normal level by the herbal extract treatment. We conclude that the herbal extract inhibits the hepatic triglyceride accumulation and stimulates alcohol metabolism by preventing ADH and ALDH from inhbition by the ethanol administration in the rat liver.

• YAKHAK HOEJI
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• v.56 no.4
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• pp.260-267
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• 2012

This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellaria baicalensis, on hepatic injury caused by ischemia/reperfusion (I/R) in alcoholic fatty liver. Rats were fed an ethanol liquid diet or a control isocaloric diet for 5 weeks, and then subjected to 60 min of hepatic ischemia and 5 h of reperfusion. Baicalin (200 mg/kg) was administered intraperitoneally 24 and 1 h before ischemia. After reperfusion, baicalin attenuated the increase in serum alanine aminotransferase activity. The levels of cytosolic cytochrome c protein expression, caspase-3 activity, the number of apoptotic cells increased after reperfusion, which were higher in ethanol-fed animals, were attenuated by baicalin. Following I/R, the hepatic lipid peroxidation was elevated, whereas hepatic glutathione content was decreased. These changes attenuated by baicalin. In ethanol-fed animals, baicalin augmented the increases in heme oxygenase-1 protein and mRNA expressions, and nuclear Nrf2 expression. In conclusion, our findings suggest that baicalin ameliorates I/R-induced hepatocellular damage by suppressing apoptosis and oxidative stress in alcoholic fatty liver.

• Journal of The Korean Society of Clinical Toxicology
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• v.2 no.1
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• pp.23-26
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• 2004

Caustic ingestion can produce a progressive and fatal injuries to esophagus, stomach and other organs. Reported exposure to acetic acid results injuries to gastrointestinal tract, hemolysis and disseminated intravascular coagulation is general, but causing hepatic necrosis by direct injuries are rare. A 47-year-old man visited our emergency medical center complaining odynophagia and abdominal pain after ingesting glacial acetic acid ($99\%$) with suicidal ideation. At the time of arrival, the patient complained mild abdominal pain but a few hours later the patient complained severe abdominal pain with markedly elevated liver enzymes. The Abdominal Computerized Tomography showed diffuse gastric wall edema and density of wedge shaped hypodense area in right hepatic dome showing focal hepatic necrosis without significant inflammation. This seems likely to be a direct effect of the noxious agent on hepatocyte involving the portal circulation.

• Journal of the East Asian Society of Dietary Life
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• v.5 no.3
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• pp.215-221
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• 1995

This study was undertaken to investigate the effect of Taraxacum herba extract on the hepatic xanthine oxidase activity as a oxygen free radical generating enzyme in vitro and in vivo. It was observed that partial purified hepatic xanthine oxidase (type O) activity was strongly inhibited by the addition of Taraxacum herba n-butanol extract in vitro. The Km value of xanthine oxidase without affecting the Vmax value for xanthine was significantly increased by the addition of ta-dase (type O) activity was significantly inhibited by the treatment of Taraxacum gerba n-butanol ex-tract for 5days(over 40mg/kg, i.p), whereas, xanthine oxidase (type D) activity was not changed by the injection of Taracacum herba n-butanol extract. Meanwhile, liver weight / body weight(%), serum alanine aminotransferase activity and hepatic lipid peroxide content in Taraxacum herba n-buta-nol extract-treated rat were not changed. These findings led us to conclude that Taraxacum herba n-butanol extract may regulate the hepatic xanthine oxidase type O activity to prevent toxic effect of oxidative stress by the oxygen free radicals.