• Clinical and Experimental Pediatrics
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• v.45 no.7
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• pp.923-927
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• 2002

Congenital hepatic fibrosis is a relatively rare disease, characterized by bile ductular proliferation and prominent fibrosis in the portal area of liver resulting in portal hypertension. It is frequently associated with other abnormalities such as polycystic kidney, Caroli syndrome, cystic dysplasia of pancreas, intestinal lymphangiectasia, pulmonary emphysema, hemangioma, and cleft palate. We report here a case of congenital hepatic fibrosis associated with renal tubular ectasia in a 3-year-old girl, whose chief complaint was abdominal distension. Her liver function test did not reveal any abnormal findings. Hepatosplenomegaly and multiple dilated bile ducts were seen in the abdominal CT scaning. Esophageal varix was not detected by an endoscopic examination. Microscopically, diffuse portal fibrosis and widening with proliferation of blie ductules in the liver specimen and tubular ectasia in renal cortex were seen.

• Molecular & Cellular Toxicology
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• v.1 no.3
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• pp.164-171
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• 2005

Toxicological studies have an object of detecting adverse effects of a chemical on an organism based on observed toxicity marker (i.e., serum biochemical markers and chemical-specific gene expression) or phenotypic outcome. To date, most toxicogenomic studies concentrated on hepatic toxicity. cDNA microarray analysis enable discrimination of the responses in animals exposed to different classes of hepatotoxicants. In an effort to further characterize the mechanisms of 2, 3, 7, 8,-Tetrachlorodibenzo-p-dioxin (TCDD or dioxin)-mediated toxicity, comprehensive temporal-responsive microarray analyses were performed on hepatic tissue from Sprague-Dawley rats treated with TCDD. Hepatic gene expression profiles were monitored using custom DNA chip containing 490 cDNA clones related with toxicology. Gene expression analysis identified 26 features which exhibited a significant change. In this study, we observed that the genes related with oxidative stress in rats exposed to Dioxin, such as CYPIIA3 and glutathione S-transferase, were up-regulated at 24hr after exposure. In this study, we carried out to discover novel evidence for previously unknown gene expression patterns related to mechanism of hepatic toxicity in rats exposed to dioxin, and to elucidate the effects of dioxin on the gene expression after exposure to dioxin.

• Asian-Australasian Journal of Animal Sciences
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• v.26 no.11
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• pp.1598-1608
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• 2013

An optimum dietary carbohydrate content is important for maximum fish growth. In this study, we fed Wuchang bream (Megalobrama amblycephala) with either control diet (30.42%) or high carbohydrate diet (52.92%) for 90 d. Fish were fed to apparent satiation three times daily in an aquarium with automatic temperature control and circulated water. Growth performance, plasma biochemical parameters, hepatic morphology and enzyme activities were determined. It was shown that compared to fish fed control diet, fish fed high carbohydrate diet had higher plasma triglyceride and cortisol levels for d 90, and lower alkaline phosphatase level for d 45, lower hepatic superoxide dismutase and total antioxidative capacity for d 90, higher malondialdehyde for d 45 and glycogen content for d 45 and 90 (p<0.05). Histological and transmission electron microscopy studies showed that hepatocytes of fish fed high carbohydrate diet contained large lipid droplets, causing displacement of cellular organelles to periphery of hepatocytes. The relative level of hepatic heat shock protein 70 (HSP70) mRNA of Wuchang bream fed high carbohydrate diet was significantly higher than that of fish fed the control diet for 90 d (p<0.05). These changes led to decreased specific growth rate and increased feed conversion ratio (p<0.05). Upon hypoxia challenge, fish fed high carbohydrate diet had higher cumulative mortality than those fed the control diet (p<0.05). These results suggested that high dietary carbohydrate (52.92%) was detrimental to the growth performance and health of Wuchang bream.

• 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.

• Toxicological Research
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• v.32 no.2
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• pp.133-140
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• 2016

Sulfasalzine is a widely administered drug against inflammatory-based disorders in human. However several cases of liver injury are associated with its administration. There is no stabilized safe protective agent against sulfasalazine-induced liver injury. Current investigation was designed to evaluate if N-acetylcysteine (NAC) and dithioteritol (DTT) as thiol reducing agents and/or vitamins C and E as antioxidants have any protective effects against sulfasalazine-induced hepatic injury in an ex vivo model of isolated rat liver. Rat liver was canulated and perfused via portal vein in a closed recirculating system. Different concentrations of sulfasalazine and/or thiol reductants and antioxidants were administered and markers of organ injury were monitored at different time intervals. It was found that 5 mM of sulfasalazine caused marked liver injury as judged by rise in liver perfusate level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) (p < 0.05). A significant amount of lipid peroxidation and hepatic glutathione depletion were detected in drug-treated livers, accompanied with significant histopathological changes of the organ. Administration of NAC ($500{\mu}M$), DTT (${400\mu}M$), Vitamin C ($200{\mu}M$), or vitamin E ($200{\mu}M$) significantly alleviated sulfasalazine-induced hepatic injury in isolated perfused rat liver. The data obtained from current investigation indicate potential therapeutic properties of thiol reductants and antioxidants against sulfasalazine-induced liver injury.

• Toxicological Research
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• v.34 no.1
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• pp.23-29
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• 2018

Ethanol-induced fat accumulation, the earliest and most common response of the liver to ethanol exposure, may be involved in the pathogenesis of liver diseases. Isoliquiritigenin (ISL), an important constituent of Glycyrrhizae Radix, is a chalcone derivative that exhibits antioxidant, anti-inflammatory, and phytoestrogenic activities. However, the effect of ISL treatment on lipid accumulation in hepatocytes and alcoholic hepatitis remains unclear. Therefore, we evaluated the effect and underlying mechanism of ISL on ethanol-induced hepatic steatosis by treating AML-12 cells with 200 mM ethanol and/or ISL ($0{\sim}50{\mu}M$) for 72 hr. Lipid accumulation was assayed by oil red O staining, and the expression of sirtuin1 (SIRT1), sterol regulatory element-binding protein-1c (SREBP-1c), AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor alpha ($PPAR{\alpha}$) was studied by western blotting. Our results indicated that ISL treatment upregulated SIRT1 expression and downregulated SREBP-1c expression in ethanol-treated cells. Similarly, oil red O staining revealed a decrease in ethanol-induced fat accumulation upon co-treatment of ethanol-treated cells with 10, 20, and $50{\mu}M$ of ISL. These findings suggest that ISL can reduce ethanol induced-hepatic lipogenesis by activating the SIRT1-AMPK pathway and thus improve lipid metabolism in alcoholic fatty livers.

• The Journal of Internal Korean Medicine
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• v.30 no.2
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• pp.306-316
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• 2009

Objectives : This study was performed to investigate the anti-fibrogenic effect of Curcumae Longae Radix on human hepatic stellate cells. Materials and Methods: Hepatic stellate cells (LX-2) were treated with various concentrations of Curcumae Longae Radix extract for 24, 48, and 72 hours. It was extracted with distilled water. After the treatment, cell viability, proliferation, cell cycle analysis, procollagen levels and the mRNA of the ASMA, TIMPl, TIMP2, MMP2, collagen type la, PDGF-receptor-beta and TGF-beta were measured by using MTT assay, BrdU assay, RT-PCR, and procollagen type 1 C-peptide EIA kit. Results : The viability of HSCs decreased in the 48 hours group, and proliferation of HSCs decreased as the concentration increased. In the cell cycle analysis, Curcumae Longae Radix decreased the ratio of M phase, and increased the ratio of apoptosis, G0/G1 and S phase. In the RT-PCR, the mRNA expression of the collagen type la and ASMA decreased with the Curcumae Longae Radix treatment. The production of procollagen by the HSCs was decreased by the treatment of Curcumae Longae Radix with high dose. Conclusion : These results suggest that Curcumae Longae Radix is helpful in the treatment of liver fibrosis as well as liver cirrhosis.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.18 no.2
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• pp.108-114
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• 2015

Purpose: The aim of this study is to evaluate the relationship between abdominal subcutaneous fat thickness measured by ultrasonography (US) and serum lipid profile and liver transaminases in obese children. Methods: One hundred and sixty-six children diagnosed with obesity from May 2001 to December 2013 were included in this study. Data on serum lipid profile and liver transaminases were collected from clinical records. Abdominal subcutaneous fat thickness and grade of hepatic steatosis were evaluated by US. Results: Of the 166 children, 107 were diagnosed with hepatic steatosis by US, 46 with grade I, 56 with grade II, and five children with grade III. According to the grade of hepatic steasosis, the average values of midline abdominal subcutaneous fat thickness and right flank abdominal subcutaneous fat thickness measured $2.9{\pm}0.8cm$ and $1.9{\pm}0.7cm$ in the normal group, $3.3{\pm}0.8cm$ and $2.0{\pm}0.7cm$ in grade I, $3.8{\pm}0.8cm$ and $2.3{\pm}0.8cm$ in grade II, and $4.1{\pm}0.8cm$ and $2.8{\pm}1.4cm$ in grade III, respectively. Abdominal subcutaneous fat thickness correlated with grade of hepatic steatosis (p<0.01). In addition, abdominal subcutaneous fat thickness correlated with concentration of serum lipids and liver transaminases in the age group of 12-14 years (p<0.01). Conclusion: Abdominal subcutaneous fat thickness measured by US can be used as a reliable predictor of possible hyperlipidemia and steatohepatitis in children, especially during the adolescent stage.

• 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.

• Korean Journal of Veterinary Research
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• v.32 no.3
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• pp.357-364
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• 1992

Artemisia Iwayomogi Compositae) has been used clinically for jaundice, hepatitis, liver cirrhosis etc. The purposes of present study were to examine pharmacological effects of Artemisia Iwayomogi water extract(AIWE) on biochemical parameters (activities of ALP and LAP, contents of glucose, total bilirubin, total protein and albumin in serum, A/G ratio, and levels of hepatic glycogen) against hepatic injury by carbon tetrachloride($CCl_4$) in rats. The results were as follows ; 1. Increased ALP activities by $CCl_4$ were very significantly(p<0.001) decreased in AIWE posttreatment groups at 72 hours and significantly(p<0.05) decreased in AIWE pretreatment groups at 72 hours. Increased LAP activities by $CCl_4$ were significantly (p<0.05) decreased in AIWE posttreatment groups at 72 hours. A little increased total bilirubin contents by $CCl_4$ were very significantly (p<0.001) decreased in AIWE posttreatment groups at 24, 48 and 72 hours. 2. Increased glucose contents by $CCl_4$ were decreased in AIWE posttreatment groups. Decreased hepatic glycogen levels by $CCl_4$, were significantly (p<0.05) increased in AIWE posttreatment groups at 48 and 72 hours. 3. Decreased total protein contents by $CCl_4$ were significantly (p<0.05) increased in AIWE posttreatment groups at 48, 72 hours. Decreased albumin contents by $CCl_4$ were increased in proportion to numbers of AIWE treatments in AIWE pre- and posttreatement groups. Decreased A/G ratios by $CCl_4$ were significantly (p<0.05) increased in AIWE posttreatment groups at 48 hours. In conclusion, AIWE did not affect normal liver function and had hepatoprotective effects rather than direct preventive effects to $CCl_4$-induced cholestasis, damages in metabolisms of glucose, protein and bilirubin.