• 동의생리병리학회지
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• 제19권5호
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• pp.1337-1343
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• 2005

The hepato-protective effects of the extract from Protaetia brevitarsis against hepatotoxicity by carbon tetrachloride ($CCI_4$) were studied in rats. The rats were orally treated with $CCI_4$ (50% in corn oil) at initial dose of $1\;m{\ell}/kg$ followed by $0.5m{\ell}/kg$ four times during 2-week period. The extract of P. brevitarsis (50, 100 or 200 mg/kg) or its vehicle was administered day after day from 1 week before $CCI_4$ Injection during five weeks. $CCI_4$ induced hepato-celluar degeneration and necrosis induced to increase in serum aspartate amintransferase (AST) and alanine aminotransferase (ALT) levels. In biochemical analyses, thiobarbituric acid-reactive substances (TBARS) and antioxidant enzymes such as superoxide dismutase (SOD) and catalase in hepatic tissues were remarkably increased by $CCI_4$ treatment. Not only increases in serum AST and ALT, but also induction of lipid peroxidation and antioxidant enzymes in hepatic tissues caused by $CCI_4$ were significantly attenuated by the P. brevitarsis extract in a dose-dependent manner. Such hepato-protective effects of P. brevitarsis extract were confirmed by histopathological examinations, wherein only mild hepatocytic vacuolations were observed in the liver of rats treated with a high dose (100 mg/kg) of P. brevitarsis extract in comparison with severe hepatocytic degenerations administered with $CCI_4$ alone. From these results, it is suggested that the extract of Protaetia brevitarsis could be a promising candidate for the protection of liver injury, based on the preventive effects against morphological cellular injuries, lipid peroxidation and serum biochemical parameters.

• 혜화의학회지
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• 제9권2호
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• pp.111-121
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• 2001

In order to evaluate the protective effect of Kamicheungkantang(KCKT) on hepatic damage induced by $CCl_4$, the study was done. The blood chemistry and histological study were done following oral administration with materials. The results were obtained as follows. 1. KCKT extracts didn't show cytotoxicity against BALB/C mouse lung fibroblast cell. 2. In the hepatotoxicity with $CCl_4$, serum alanine aminotransferase(ALT) was significantly decreased in KCKT treated group as compared with control group. 3. In the hepatotoxicity with $CCl_4$, serum aspartate aminotransferase (AST) was significantly decreased in KCKT treated group as compared with control group. 4. In the hepatotoxicity with $CCl_4$, serum alkaline phosphatase(ALP) was significantly decreased in KCKT treated group as compared with control group. 5. In the hepatotoxicity with $CCl_4$, serum lactate dehydrogenase(LDH> was insignificantly decreased in KCKT but insignificantly as compared with control group. 6. In the hepatotoxicity with $CCl_4$, serum cholestorol was significantly decreased in KCKT treated group as compared with control group. 7. In the hepatotoxicity with $CCl_4$, serum triglyceride was insignificantly decreased in KCKT treated groups as compared with data of control. 8. In the hepatotoxicity with $CCl_4$, serum total bilirubin, direct bilirubin, ${\gamma}$-GTP were not changed in KCKT treated groups as compared with data of control. 9. In histopathological changes, fatty changes, vacuole, nucleotic changes and fibrosis were observed in control group and degree of changes was increased over time. Whereas no differences were observed in KCKT treated group These results suggested that KCKT extracts might be usefully applied for treatment of hapatic disease and also it was necessary to do more studies about its mechanisms.

• Nutrition Research and Practice
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• 제12권6호
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• pp.535-540
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• 2018

BACKGROUND/OBJECTIVES: Propolis has a rich source of bioactive compounds and has renal and hepatic protective properties. The purpose of this study was to investigate the beneficial effect of hydro-ethanolic extract of propolis against paracetamol-induced liver damage and impairment of kidney function, as well as hematological changes in rats. MATERIALS/METHODS: Six groups of rats were used; the first group was served as a control; the second and third groups were treated by propolis extract at a dose of 50 and 100 mg/kg.B.WT. respectively; the fourth group was treated by paracetamol (200 mg/kg.B.WT.); the fifth group was treated by propolis (50 mg/kg.B.WT.) for eight days and then received similar dose of propolis for following seven days with paracetamol at a dose of 200 mg/kg.B.WT. daily for the seven days; and the sixth group was treated with propolis (100 mg/kg.B.WT.) for eight days and then received similar dose of propolis for following seven days with paracetamol at a dose of 200 mg/kg.B.WT. daily for the seven days. All the animals were treated for a period of 15 days. At the end of the experimental period, blood samples were collected for measurement of the liver enzymes, serum albumin, protein and creatinine, blood urea nitrogen, hematological parameters, and urine volume, protein and albumin. RESULTS: Paracetamol over dose significantly lowered hemoglobin, serum total protein, albumin, and uric acid, while it significantly increased blood creatinine, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase activities, white blood cells, and platelet count as compared to the control. However, these alterations were significantly attenuated by the use of propolis extract and the effect was dose dependent. Interestingly, propolis prevented paracetamol induced proteinuria, low hemoglobin and body weight loss. CONCLUSIONS: Propolis significantly prevented paracetamol induced renal, hepatic and hematological toxicity and might be useful in the management of liver and renal diseases particularly proteinuria.

• 대한임상독성학회지
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• 제16권2호
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• pp.108-115
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• 2018

Purpose: Glehnia littoralis has been reported to have several pharmacological properties but no in vivo reports describing the protective effects of this plant on${\alpha}$-amanitin-induced hepatotoxicity have been published. ${\alpha}$-Amanitin is a peptide found in several mushroom species that accounts for the majority of severe mushroom poisonings leading to severe hepatonecrosis. In our previous in vitro study, we found that ${\alpha}$-amanitin induced oxidative stress, which may contribute to its severe hepatotoxicity. The aim of this study was to investigate whether Glehnia littoralis acetate extract (GLEA) has protective antioxidant effects on ${\alpha}$-amanitin-induced hepatotoxicity in a murine model. Methods: Swiss mice (n=40 in all groups) were divided into four groups (n=10/group). Three hours after giving ${\alpha}$-amanitin (0.6 mg/kg, i.p.) to the mice, they were administered silibinin (50 mg/kg/d, i.p.) or Glehnia littoralis ethyl acetate extract (100 mg/kg/d, oral) therapies once a day for 3 days. After 72 hours of treatment, each subject was killed, cardiac blood was aspirated for hepatic aminotransferase measurement, and liver specimens were harvested to evaluate the extent of hepatonecrosis. The degree of hepatonecrosis was assessed by a pathologist blinded to the treatment group and divided into 4 categories according to the grade of hepatonecrosis. Results: GLEA significantly improved the beneficial functional parameters in ${\alpha}$-amanitin-induced hepatotoxicity. In the histopathological evaluation, the toxicity that was generated with ${\alpha}$-amanitin was significantly reduced by GLEA, showing a possible hepatoprotective effect. Conclusion: In this murine model, Glehnia littoralis was effective in limiting hepatic injury after ${\alpha}$-amanitin poisoning. Increases of aminotransferases and degrees of hepatonecrosis were attenuated by this antidotal therapy.

• 한국식품영양과학회지
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• 제30권5호
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• pp.928-932
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• 2001

노루궁뎅이 버섯의 간 손상 억제 작용을 확인하고자 B($\alpha$)P투여로 간 독성이 유발된 마우스에서 과산화지질의 생성, 항산화에 관련된 효소 및 물질의 변화를 살펴본 결과, B($\alpha$)P투여로 인해 혈청 ALT와 AST의 활성, 간조직 중의 과산화지질 함량, cytochrome P450 함량, SOD, catalase 그리고 GSH-Px의 활성이 유의적으로 증가하였고, GSH함량과 GST활성은 감소하였다. 반면 노루궁뎅이 버섯 메탄올 추출물의 전처리로 인해 ALT 와 AST의 활성, 과산화지질 함량, cyto-chrome P450 함량 그리고 항상화효소인 SOd, catalase 및 GSH-Px의 활성이 유의적으로 감소하였으며 GSH 함량과 GST 활성은 증가하였다. 그리고 마우스의 간 조직에서 cyto-chrome P450 1Al isozyme의 단백질 발현을 western blotting 으로 조사한 결과, B($\alpha$)P투여로 대조군에 비해 현저히 증가한 단백질 발현이 노루궁뎅이 버섯 메탄올 추출물을 투여함으로써 감소됨을 확인하였다. 이상의 결과로 노루궁뎅이 버섯 메탄올 추출물은 생체 내에서 자유기로 인해 야기되는 간장의 산화적 손상을 효과적으로 억제할 수 있을 것으로 사료된다.

• Nutrition Research and Practice
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• 제7권4호
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• pp.273-280
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• 2013

Bamboo salt, a Korean folk medicine, is prepared with solar salt (sea salt) and baked several times at high temperatures in a bamboo case. In this study, we compared the preventive effects of bamboo salt and purified and solar salts on hepatic damage induced by carbon tetrachloride in Sprague-Dawley rats. Compared with purified and solar salts, bamboo salts prevented hepatic damage in rats, as evidenced by significantly reduced serum levels of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase (P < 0.05). Bamboo salt (baked $9{\times}$) triggered the greatest reduction in these enzyme levels. In addition, it also reduced the levels of the proinflammatory cytokines interleukin (IL)-6, interferon (IFN)-${\gamma}$, and tumor necrosis factor (TNF)-${\alpha}$. Histopathological sections of liver tissue demonstrated the protective effect of bamboo salt, whereas sections from animals treated with the other salt groups showed a greater degree of necrosis. We also performed reverse transcription-polymerase chain reaction and western blot analyses of the inflammation-related genes iNOS, COX-2, TNF-${\alpha}$, and IL-$1{\beta}$ in rat liver tissues. Bamboo salt induced a significant decrease (~80%) in mRNA and protein expression levels of COX-2, iNOS, TNF-${\alpha}$, and IL-$1{\beta}$, compared with the other salts. Thus, we found that baked bamboo salt preparations could prevent $CCl_4$-induced hepatic damage in vivo.

• 운동과학
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• 제26권3호
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• pp.223-228
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• 2017

PURPOSE: This study investigated the protective role of high-intensity interval training against acute liver injury induced by D-galactosamine (D-Gal)/lipopolysaccharide (LPS). METHODS: A total of 30 male BALB/c mice aged 5-week were randomly assigned to high-intensity, interval training group (EX, n=10) or control group in cage (Non-EX, n=20) for 10 weeks. Peritoneal injection of D-Gal (700 mg/kg body weight) and LPS ($10{\mu}g/kg$ body weight) was applied to induce acute liver injury, and liver tissue was harvested 6 hours after the injection. Hematoxylin and Eosin (H&E) staining was used for liver histology. Real-time PCR was used to quantify expression of pro-inflammatory and anti-inflammatory genes in the liver. RESULTS: The liver histology showed that D-Gal/LPS treatment resulted in hepatic damage and increased number of neutrophils in conjunction with upregulation of hepatic IL-6 and $TNF-{\alpha}$ mRNAs and downregulation of hepatic $PPAR{\alpha}$ and SIRT1 mRNAs. On the other hand, the 10-week interval training resulted in a significant improvement in cardiorespiratory fitness assessed as run time to exhaustion on a treadmill. In addition, the interval training attenuated the D-Gal/LPS-induced liver damage and increased number of neutrophil in conjunction with downregulation of hepatic IL-6 and $TNF-{\alpha}$ mRNAs and upregulation of hepatic $PPAR{\alpha}$ and SIRT1 mRNAs. CONCLUSIONS: This study suggests that high-intensity interval training suppresses the D-Gal and LPS-induced acute liver damage and inflammatory responses.

• Nutrition Research and Practice
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• 제4권3호
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• pp.191-195
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• 2010

There is an increasing interest in curcumin (Curcuma longa L.) as a cardiovascular disease (CVD) protective agent via decreased blood total cholesterol and low-density lipoprotein-cholesterol (LDL-cholesterol) level. The aim of this study was to investigate further the potential mechanism in the hypocholesterolemic effect of curcumin by measuring cholesterol 7a-hydroxylase (CYP7A1), a rate limiting enzyme in the biosynthesis of bile acid from cholesterol, at the mRNA level. Male Sprague-Dawley rats were fed a 45% high fat diet or same diet supplemented with curcumin (0.1% wt/wt) for 8 weeks. The curcumin diet significantly decreased serum triglyceride (TG) by 27%, total cholesterol (TC) by 33.8%, and LDL-cholesterol by 56%, respectively as compared to control group. The curcumin-supplemented diet also significantly lowered the atherogenic index (AI) by 48% as compared to control group. Hepatic TG level was significantly reduced by 41% in rats fed with curcumin-supplemented diet in comparison with control group (P < 0.05). Conversely, the curcumin diet significantly increased fecal TG and TC. The curcumin diet up-regulated hepatic CYP7A1 mRNA level by 2.16-fold, compared to control group p (P < 0.05). These findings suggested that the increases in the CYP7A1 gene expression may partially account for the hypocholesterolemic effect of curcumin.

• 한국식품영양과학회지
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• 제28권6호
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• pp.1364-1368
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• 1999

This study was carried out to investigate the inhibiton effects of Coprinus comatus ethanol extract of edible mushroom on liver damage in benzo(a)pyrene (B(a)P) treated mice. The activities of serum aminotransferase, cytochrome P 450 and hepatic content of lipid peroxide after B(a)P treatment were increased than those of control, but those levels were significantly decreased by the treatment of Coprinus comatus ethanol extract. Whereas, the hepatic glutathione content and glutathione S transferase activity were decreased by B(a)P treatment than those of control, but those were increased by the treatment of Coprinus comatus ethanol extract. Also the activities of superoxide dismutase, catalase and glutathione peroxidase after B(a)P treatment were markedly increased than those of control, but those levels were decreased by the treatment of Coprinus comatus ethanol extract. These results suggest that Coprinus comatus ethanol extract have a protective effect on liver damage by benzo(a)pyrene through the mechanisms of decreasing lipid peroxide and activities of free radical generating enzymes.

• 동의생리병리학회지
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• 제16권4호
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• pp.707-713
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• 2002

Astragali radix (AR) is one of the oldest and mast frequently used crude drug for traditional medicine in many Asian countries. This study designed to investigate the hepatoprotective effects of the aqueous extracted AR (ARE) against acetaminophen (APAP)-induced hepatic damage in ICR mice. APAP at the dose of 450 mg/kg i.p produced liver damage in ICR mice. Serum enzyme activities of alanine aminotransferase, aspartate aminotransferase and sorbitol dehydrogenese was dramatically decreased up to control level by pretreatment of ARE. However, hepatic glutathione level did not show a significant change between the tested groups. We also investigated TNF α mRNA gene expression on APAP-induced liver damage by RT-PCR. APAP dramatically induced TNF α mRNA gene expression in ICR mice. Pretreatment of mice with ARE led to a marked decrease of TNF α mRNA gene expression. These data indicate that 1) ARE has clearly revealed a hepatoprotective effect against APAP-induced hepatic damage in ICR mice, and 2) the protective effect of ARE may be, in part, associated with the regulation of TNF α mRNA gene expression.