• Title/Summary/Keyword: Hepatic necrosis

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Preventive Effect of the Korean Traditional Health Drink (Taemyeongcheong) on Acetaminophen-Induced Hepatic Damage in ICR Mice

  • Yi, Ruo-Kun;Song, Jia-Le;Lim, Yaung-Iee;Kim, Yong-Kyu;Park, Kun-Young
    • Preventive Nutrition and Food Science
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    • v.20 no.1
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    • pp.52-59
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    • 2015
  • This study was to investigate the preventive effect of taemyeongcheong (TMC, a Korean traditional health drink) on acetaminophen (APAP, 800 mg/kg BW)-induced hepatic damage in ICR mice. TMC is prepared from Saururus chinensis, Taraxacum officinale, Zingiber officinale, Cirsium setidens, Salicornia herbacea, and Glycyrrhizae. A high dose of TMC (500 mg/kg BW) was found to decrease APAP-induced increases in serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase. TMC pretreatment also increased the hepatic levels of hepatic catalase, superoxide dismutase, glutathione peroxidase, and glutathione, and reduced serum levels of the inflammatory cytokines tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-6 in mice administered APAP (P<0.05). TMC (500 mg/kg BW) reduced hepatic mRNA levels of TNF-${\alpha}$, IL-$1{\beta}$, IL-6, COX-2, and iNOS by 87%, 84%, 89%, 85%, and 88%, respectively, in mice treated with APAP (P<0.05). Furthermore, histological observations suggested TMC pretreatment dose-dependently prevented APAP-induced hepatocyte damage. These results suggest that TMC could be used as a functional health drink to prevent hepatic damage.

Clinico-biochemical Study on Experimental Partial and Complete Obstruction of the Common Bile Duct in Korean Goats (한국염소에서 실험적 총담관부분 및 완전폐쇄에 따른 임상생화학적 연구)

  • Yoo Ra-Gyeong;Cheong Jong-Tae;Nam Tchi-Chou
    • Journal of Veterinary Clinics
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    • v.8 no.1
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    • pp.71-80
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    • 1991
  • Clinical signs, serum chemical values and histological findings of hepatic tissue after partial and complete obstruction of common bile duct in Korean goats were investigated. Abnormal clinical signs were not observed in partial obstruction of common bile duct, but in complete obstruction clinical signs such as jaundice, urine color change, were observed. Serum total bilirubin, total cholesterol, aspartate aminotransferase, sorbitol dehydrogenase, gamma glutamyltranspeptidase, and total protein values increased on the 1-4th day and then gradually decreased to normal level in partial obstruction. However, they tend to increase persistently by the 24th day in complete obstruction of common bileduct. Histologic features of hepatic tissue in partial obstruction were not changed as compared with normal hepatic tissue. On the other hand, in complete obstruction of common bite duct there were moderate bile duct proliferation in a portal area, rupture of bile canaliculi, phagocytosis of bile pigment by Kupffer cells, periportal fibrosis, intrahepatic bile stasis and hepatic cell necrosis.

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Outcome of Extended Porta Hepatis Dissection and Hepatic Portojejunostomy for Biliary Atresia (담도 폐쇄증에서 광범위 간문부 절제 및 간문부-공장 문합술의 치료성적)

  • Lee, Seong-Cheol
    • Advances in pediatric surgery
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    • v.3 no.2
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    • pp.93-97
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    • 1997
  • Extended porta hepatis dissection and hepatic portojejunostomy was performed on 14 biliary atresia patients during last 13 years by a single surgeon. The average age at operation was 68 days(range from 37 days to 98 days). The patients were admitted for 8 weeks postoperatively for administration of parenteral antibiotics. There was one operative mortality due to acute hepatic necrosis. Among 13 patients remaining, 12(92.5 %) became chemically jaundice-free within 36 weeks postoperatively(average 16.8 weeks). the earliest 8 weeks, and in one patients jaundice persisted. Five(38.5 %) patients developed cholangitis after operation. Among jaundice-free patients, one patient died of unrelated disease 2 years after hepatic portojejunostomy, who underwent left lateral segmentectomy because of a biloma. Eleven survivors(78.6 %) are jaundice-free. The oldest one is 13 years old, enjoying a normal life. The mean period of follow-up is 7 years and 3 months.

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Acute Hepatic Failure Induced by Xylitol Toxicosis in Two Dogs

  • Lim, Chae-Young;Yoo, Jong-Hyun;Kim, Chun-Geun;Park, Chul;Park, Hee-Myung
    • Journal of Veterinary Clinics
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    • v.25 no.6
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    • pp.510-513
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    • 2008
  • Two dogs were referred due to vomiting, depression and anorexia after ingestion of xylitol gum. Both dogs were presented with hepatic failure and one dog had concurrent renal failure. Aggressive supportive treatment was performed, but these dogs died. Necropsy of one dog revealed acute hepatic necrosis, severe renal damages, and hemoperitoneum. This case report demonstrates potential hazard of xylitol toxicity for dogs with clinicopathological and pathological findings.

Influence of Thyroxine on the Hepatotoxicity of Carbon Tetrachloride ($CC1_4$의 간장독작용(肝臟毒作用)에 미치는 Thyroxine의 영향(影響))

  • Hong, Ki-Sung;Cheon, Yun-Sook
    • The Korean Journal of Pharmacology
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    • v.16 no.2 s.27
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    • pp.31-38
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    • 1980
  • Calvert et al. formulated the hypothesis that carbon tetrachloride ($CCl_4$) acted on the central nervous system to produce and intensify sympathetic discharge which resulted in anoxic necrosis of the liver. Recknagel suggested that the essential feature of $CCl_4$ hepatotoxicity depended on the cleavage of it to $CCl_3$(free radical) and the peroxidative decomposition of cytoplasmic membrane structural lipids. And there are many reports which show the increase of adrenergic activity in hyperthyroidism. In this paper, the influence of thyroxine on the hepatotexicity of carbon tetrachloride was investigated in mice. The results obtained were summarized as follows; 1) Hepatic total lipid and lipid peroxide contents were slightly decreased by L-sodium thyroxine injection(4mg/kg/day for 4days or 6days), but hepatic glycogen content was significantly decreased. 2) Hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity were significantly increased by $CCl_4$ (4 ml/kg single dose or triple dose: 4ml/kg/day for 3days), but hepatic glycogen content was significantly decreased. 3) The increase of hepatic total lipid and lipid peroxide contents and serum lactic dehydrogenase activity induced by $CCl_4$ were significantly inhitited by the pretreatment of thyroxine. 4) The decrease of hepatic glycogen induced by $CCl_4$ was not affected by the pretreatment of thyroxine.

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A Case of Hepatocellular Carcinoma after Hepatic Artery Ligation (간동맥 결찰 환자에서 발생한 간세포암 1례)

  • Suh, Jeong-Il;Kim, Joon-Hwan;Lee, Dong-Joon;Kim, Ki-Yoon;Kang, Ho-Jung;Park, Chan-Won;Lee, Heon-Ju
    • Journal of Yeungnam Medical Science
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    • v.13 no.1
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    • pp.146-151
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    • 1996
  • Majority of hepatocellular carcinoma is evolved from a well differentiated cancerous condition such as hyperplastic lesions eg. adenomatous hyperplasia in cirrhotic liver or de no vo carcinogenesis and prolifenation along with dedifferentiation. Adenomatous hyperplasia is may be seen in severe acute hepatic injury, like submassive hepatic necrosis, or in chronic liver diseases, particularly liver cirrhosis and it has recently attracted much interest from both clinicians and pathologists because it is regarded as a precursor lesion of hepatocellular carcinoma. Hepatic adenomatous hyperplasia resembling focal nodular hyperplasia might have developed from localized vascular changes associated with chronic liver disease, pre-existing arterial malformation and early stage of angiogenesis in hepatocarcinogenesis. We present a patient who developed hepatocellular carcinoma after hepatic artery ligation.

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Hepatoprotection by Semisulcospira libertina against Acetaminophen-Induced Hepatic Injury in Mice

  • Jeon, Tae-Won;Lee, Young-Sun;Kim, Hyo-Jung
    • Preventive Nutrition and Food Science
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    • v.8 no.3
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    • pp.239-244
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    • 2003
  • Recently, we reported (J Korean Soc Food Sci Nutr, 31(3): 516-520, 2002) that Semisulcospira libertina (Marsh Snail) pretreatment has a hepatoprotective effect on $CCl_4$-induced liver damage in rats. The purpose of this study was to investigate the possible mechanisms of hepatoprotection by S. libertina (SL) on liver injury induced by acetaminophen (AA). Male ICR mice were pretreated with dehydrated powder of SL once daily for three consecutive days, given a single toxic dose of AA (450 mg/kg) and liver function determined 24 h later. Liver damage was assessed by quantifying serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and sorbitol dehydrogenase (SDH) activities, and by measuring hepatic lipid peroxidation. To confirm possible mechanism(s), the content of hepatic glutathione (GSH) and gene expression of tumor necrosis factor a (TNF $\alpha$) mRNA by reverse transcription-polymerase chain reaction (RTPCR) were also measured. Pretreatment with SL dramatically lowered AA-elevated ALT, AST and SDH activities. SL pretreatment decreased AA-produced lipid peroxidation by 11% and restored the AA-depleted hepatic GSH by 27%. Furthermore, SL markedly suppressed the expression of TNF $\alpha$ mRNA induced by AA. Our findings revealed that the possible hepatoprotective mechanisms of SL could be attributed, at least in part, to the glutathione-mediated detoxification as well as the regulation of TNF $\alpha$ mRNA expression.

Acanthopanax koreanum Nakai modulates the immune response by inhibiting TLR 4-dependent cytokine production in rat model of endotoxic shock

  • Jung, Myung-Gi;Do, Gyeong-Min;Shin, Jae-Ho;Ham, Young Min;Park, Soo-Yeong;Kwon, Oran
    • Nutrition Research and Practice
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    • v.7 no.6
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    • pp.460-465
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    • 2013
  • The hepatoprotective activity of Acanthopanax koreanum Nakai extract (AE) was investigated against D-Galactosamine/Lipopolysaccharide (D-GalN/LPS)-induced liver failure rats compared with that of acanthoic acid (AA) isolated from AE. Although D-GalN/LPS (250 mg/kg body weight/$10{\mu}g/kg$ body weight, i.p.) induced hepatic damage, pretreatments with AE (1 and 3% AE/g day) and AA (0.037% AA, equivalent to 3% AE/g day) alleviated the hepatic damage. This effect was the result of a significant decrease in the activity of alanine transaminase. Concomitantly, both the nitric oxide and IL-6 levels in the plasma were significantly decreased by high-dose AE (AE3) treatment compared to the GalN/LPS control (AE0). This response resulted from the regulation of pro-inflammatory signaling via a decrease in TLR4 and CD14 mRNA levels in the liver. While a high degree of necrosis and hemorrhage were observed in the AE0, pretreatment with AE3 and AA reduced the extent of hepatocyte degeneration, necrosis, hemorrhage and inflammatory cell infiltrates compared to the AE0. In conclusion, these results suggest that especially high-dose AE are capable of alleviating D-GalN/LPS-induced hepatic injury by decreasing hepatic toxicity, thereby mitigating the TLR 4-dependent cytokine release. The anti-inflammatory effect of AE could be contributing to that of AA and AE is better than AA.

Combined Treatment of Silymarin and Jakyakgamcho-tang Suppresses Hepatic Lipid Accumulation and Inflammation in C57BL/6 Mice (Silymarin과 작약감초탕 병용투여의 C57BL/6 마우스 간조직 지질축적 및 염증 억제효과)

  • Choi, Jeong Won;Cho, Su-Jung;Shin, Mi-rae;Park, Hae-Jin
    • The Korea Journal of Herbology
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    • v.37 no.5
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    • pp.17-26
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    • 2022
  • Objective : The aim of the present study is to examine hepatic lipid-lowering and anti-inflammatory effects of silymarin combined with Jakyakgamcho-tang on non-alcoholic fatty liver disease in a high fat diet-induced obese mice model. Methods : C57BL/6 mice were divided into four dietary groups: (1) Normal, (2) Control (60% high-fat diet), (3) Control + silymarin 50 mg/kg/day (Silymarin), (4) Control + Silymarin 50 mg/kg/day + Jakyakgamcho-tang 100 mg/kg/day (SPG). After 12 weeks administration, mice were sacrificed and lipids and inflammation-related biomarkers were analyzed liver and plasma. Results : Silymarin and SPG treatments significantly lowered body and liver weights compared to the Control. Serumlipids (triglyceride (TG), total cholesterol) and pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin 1𝛽, and IL-6) concentrations were significantly lowered in the Silymarin and SPG groups than the Control group. Silymarin and SPG treatments suppressed hepatic TG level and hepatic lipid droplets compared to the Control. Theses two treatments significantly increased hepatic kinase B1 and AMP-activated protein kinase protein levels, and significantly decreased hepatic key lipogenic enzymes (acetyl-CoA carboxylase, fatty acid synthase and stearyl coenzyme A desaturase 1) protein levels than the Control. SPG also significantly increased hepatic fatty acid oxidation-related protein (peroxisome proliferator-activated receptor alpha and uncoupling protein 2) levels than the Control. Conclusions: Silymarin and SPG suppressed hepatic lipid accumulation by regulating hepatic protein expression, and lowered blood pro-inflammatory cytokines concentrations though the synergic effect of silymarin and Jakyakgamchotang was not clear.

Protective Effects of Monosodium-L-Glutamate on the Fatty Liver induced by Carbon Tetrachloride in Rat (사염화탄소-유발지방간에 대한 L-글루탐산 일나트륨의 보호작용)

  • Kim, Hyoung-Chun;Lee, Wang-Seop;Chun, Wan-Jhoo;Choi, Yong-Soon;Kim, Soo-Hee;Lee, Hyun-Woo;Jhoo, Wang-Kee
    • YAKHAK HOEJI
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    • v.36 no.1
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    • pp.73-79
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    • 1992
  • To achieve better understanding of the effects of monosodium-L-glutamate(MSG) against $CCl_4$ fatty liver in Wister male rats, 5% MSG solution was given as drinking water and $CCl_4$ 0.1 ml/kg was injected subcutaneously twice a week for four weeks. It was showed that increased hepatic phospholipid and hepatic triacylglycerol levels by $CCl_4$ challenge were significantly decreased by additionnal MSG, respectively. However, MSG had no apparent effect on the elevated hepatic cholesterol level in the presence of $CCl_4$. Histologically, additional MSG markedly inhibited fatty degeneration, spotty necrosis, inflammation and periportal vascular proliferation manifested by $CCl_4$. respectively. These results indicated that effects of MSG against $CCl_4$ induced-fatty liver appeared to be involved with partial restoration of altered hepatic lipid composition.

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