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      Monocrotaline으로 유발된 흰쥐의 간독성에 대한 해독정기탕의 효과 = Effect of Haedokjeongki-tang in Rat Liver after Monocrotaline Exposure

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      https://www.riss.kr/link?id=A100571538

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      다국어 초록 (Multilingual Abstract)

      Monocrotaline (MCT) is a pyrrolizidine alkaloid (PA) plant toxin that produces hapatotoxicity in humans and animals. To felt the hypothesis, we investigated the possible protective effects of Haedokjeongki-tang as an antioxidant against MCT-induced liver injury in rats. Cells with apoptotic morphology have been observed in the livers of animals exposed to Ph and Haedokjeongki-tang. Whether apoptosis occurs in the livers of MCT-treated animals and whether it is required for full manifestation of pathological changes is not known, To determine this, rats were treated with 100 mg MCT/kg, and apoptosis was detected by transmission electron microscopy and TUNEL assay. MCT produced apoptosis in the liver by 6 h after treatment and increased by 24 h. Administration of Haedokjeongki-tang did affect liver structure and inhibit apopotosis in MCT-induced liver injury. Upon light and electron microscopic examination, we observed that Haedokjeongki-tang improved the morphological and histopathological changes of the liver caused by MCT-induced injury. MCT caused a time-dependent release of GOT and GPT, a marker of liver injury. Furthermore, we observed with respect to antioxidants status, catalase and superoxide dismutase activity tended to be higher in the MCT-treated rats than in the Haedokjeongki-tang administered rats. Our finding showed that Haedokjeongki-tang administration partially reduced liver injury after MCT exposure.
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      Monocrotaline (MCT) is a pyrrolizidine alkaloid (PA) plant toxin that produces hapatotoxicity in humans and animals. To felt the hypothesis, we investigated the possible protective effects of Haedokjeongki-tang as an antioxidant against MCT-induced li...

      Monocrotaline (MCT) is a pyrrolizidine alkaloid (PA) plant toxin that produces hapatotoxicity in humans and animals. To felt the hypothesis, we investigated the possible protective effects of Haedokjeongki-tang as an antioxidant against MCT-induced liver injury in rats. Cells with apoptotic morphology have been observed in the livers of animals exposed to Ph and Haedokjeongki-tang. Whether apoptosis occurs in the livers of MCT-treated animals and whether it is required for full manifestation of pathological changes is not known, To determine this, rats were treated with 100 mg MCT/kg, and apoptosis was detected by transmission electron microscopy and TUNEL assay. MCT produced apoptosis in the liver by 6 h after treatment and increased by 24 h. Administration of Haedokjeongki-tang did affect liver structure and inhibit apopotosis in MCT-induced liver injury. Upon light and electron microscopic examination, we observed that Haedokjeongki-tang improved the morphological and histopathological changes of the liver caused by MCT-induced injury. MCT caused a time-dependent release of GOT and GPT, a marker of liver injury. Furthermore, we observed with respect to antioxidants status, catalase and superoxide dismutase activity tended to be higher in the MCT-treated rats than in the Haedokjeongki-tang administered rats. Our finding showed that Haedokjeongki-tang administration partially reduced liver injury after MCT exposure.

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      참고문헌 (Reference)

      1 "production and role in the kidney" 765-776, 1986

      2 Kim SY, "The effect of betaine on the CCl4-induced hepatoxicity in rats" 538-543, 1993

      3 Reitman FA, "Studies on calcium transport during carbon tetrachloride mediated hepatotoxicity in mice" 4584-6, 1988

      4 Beers RJ, "Spectrophotometric method for measuring the breakdown of H2O2 by catalase" 133-140, 1952

      5 Schoental R, "Pathological changes in rats as a result of treatment with monocrotaline" 229-237, 1955

      6 Brayan LC, "Modes of cell death in rat liver after monocrotalin exposure" 77 : 172-182, 2004

      7 Gujral JS, "Mode of cell death after acetaminophen overdose in mice" 67 : 322-328, 2002

      8 Willson DW, "Mechanism and pathology of monocrotaline pulmonary toxicity" 307-325, 1992

      9 Copple BL, "Liver inflammation during monocrotaline hepatotoxicity" 190 : 155-169, 2003

      10 Schumann J, "Importance of Kupffer cells for T-cell dependent liver injury in mice" 157 : 1671-1683, 2000

      1 "production and role in the kidney" 765-776, 1986

      2 Kim SY, "The effect of betaine on the CCl4-induced hepatoxicity in rats" 538-543, 1993

      3 Reitman FA, "Studies on calcium transport during carbon tetrachloride mediated hepatotoxicity in mice" 4584-6, 1988

      4 Beers RJ, "Spectrophotometric method for measuring the breakdown of H2O2 by catalase" 133-140, 1952

      5 Schoental R, "Pathological changes in rats as a result of treatment with monocrotaline" 229-237, 1955

      6 Brayan LC, "Modes of cell death in rat liver after monocrotalin exposure" 77 : 172-182, 2004

      7 Gujral JS, "Mode of cell death after acetaminophen overdose in mice" 67 : 322-328, 2002

      8 Willson DW, "Mechanism and pathology of monocrotaline pulmonary toxicity" 307-325, 1992

      9 Copple BL, "Liver inflammation during monocrotaline hepatotoxicity" 190 : 155-169, 2003

      10 Schumann J, "Importance of Kupffer cells for T-cell dependent liver injury in mice" 157 : 1671-1683, 2000

      11 Huxtable RJ, "Human health implications of PA and herbs containing them In Toxicant of plant Origin 1" 41-86, 1989

      12 Shi J, "Evidence of hepatocyte apoptosis in rat liver after the administration of carbon tetrachloride" 153 : 515-525, 1998

      13 Mattocks AR, "Estimation of metabolites of PA in animal tissues" 529-535, 1970

      14 Hongo M, "Effects of nicorandil on monocrotaline-induced pulmonary arterial hypertension in rats" 46 : 452-458, 2005

      15 Meyrick BW, "Development of crotalaria pulmonary hypertention" 692-702, 1980

      16 Schultz AE, "Chronic pulmonary hypertension: The monocrotaline model and involvement of the hemostatic system" 1 : 271-346, 1998

      17 Corcoran GB, "Buttyan R; Contemporary in toxicology molecular control point in toxicity" 169-181, 1994

      18 Janssen YMW, "Biology of disease cell and tissue responses to oxidative damage" 261-274, 1993

      19 Gorden GJ, "Bax-mediated apoptosis in the livers of rat after hepatectomy in the retrorsine model of hepatocellular injury" 32 : 312-320, 2000

      20 Yacoub LK, "Apoptosis and bcl-2 protein expression in experimental alcoholic liver disease in the rat" 19 : 854-859, 1995

      21 Copple BL, "Anticoagulants prevent monocrotaline-induced hepatic parenchymal cell injury but not endothelial cell injury in the rat" 180 : 186-196, 2002

      22 Deng HL, "Anti-lipid peroxidative effect of ginsenoside Rb1 and Rg1" 1991

      23 Jaeschke H, "Activation of caspase 3-like proteases is essential for TNF-alpha induced hepatic parenchymal cell apoptosis and neutrophil-mediated necrosis in a murine endotoxin shock model" 160 : 3480-3486, 1998

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2022 평가예정 재인증평가 신청대상 (재인증)
      2019-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2018-12-01 평가 등재후보로 하락 (계속평가) KCI등재후보
      2015-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2014-03-17 학술지명변경 외국어명 : Korean Journal of Microscopy -> Applied Microscopy KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-09-22 학술지명변경 한글명 : 한국전자현미경학회지 -> 한국현미경학회지
      외국어명 : Korean Journal of Electron Microscopy -> Korean Journal of Microscopy
      KCI등재
      2007-10-24 학회명변경 한글명 : 한국전자현미경학회 -> 한국현미경학회
      영문명 : Korean Society Of Electron Microscopy -> Korean Society Of Microscopy
      KCI등재
      2007-01-01 평가 등재 1차 FAIL (등재유지) KCI등재
      2004-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2003-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2002-01-01 평가 등재후보학술지 유지 (등재후보1차) KCI등재후보
      1999-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.11 0.11 0.12
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.12 0.12 0.273 0
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