• Journal of Yeungnam Medical Science
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• v.40 no.2
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• pp.115-122
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• 2023

Hepatic ischemia-reperfusion injury is a major complication of liver transplantation, trauma, and shock. This pathological condition can lead to graft dysfunction and rejection in the field of liver transplantation and clinical hepatic dysfunction with increased mortality. Although the pathological mechanisms of hepatic ischemia-reperfusion injury are very complex, and several intermediators and cells are involved in this phenomenon, oxidative stress and inflammatory responses are the key processes that aggravate hepatic injury. This review summarizes the current understanding of oxidative stress and inflammatory responses and, in that respect, addresses the therapeutic approaches to attenuate hepatic ischemia-reperfusion injury.

• Investigative Magnetic Resonance Imaging
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• v.16 no.1
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• pp.76-80
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• 2012

Eosinophilic infiltration in the liver is not a rare disease and it is usually presented as multiple, small, ill defined, oval or round, low attenuated lesions on portal phase of computed tomography. We reported case of hepatic eosinophilic infiltration in the liver, as an unusual manifestation of segmental involvement.

• Biomedical Science Letters
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• v.18 no.3
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• pp.276-282
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• 2012

High-intensive endurance exercises induce cell changes in body, changes in structures and functions of the heart, the muscles, the cartilages, and the liver, as well as increase of inflammatory cytokine. The purpose of this study was to estimate the biochemical changes in the liver and muscles during ultra-marathon race (100 km) by sections. The blood of the subjects was collected before the marathon as a control in order to analyze serum creatine kinase (CK), lactic dehydrogenase (LDH), asprtate aminotransferase (AST), alanine aminotransferase (ALT), total(T)-bilirubin, direct(D)-bilirubin, total protein, albumin, uric acid, gamma-glutamyltranspeptidase (${\gamma}$-GTP), alkaline phosphatase (ALP), creatinine, blood urea nitrogen (BUN), and high sensitive C-reactive protein (hs-CRP) concentrations. The CK, LDH, D-bilirubin, AST and ALT concentrations at 50 km and 100 km were significantly increased compared to the control (P<0.05). The markers at 100 km were higher than those at 50 km (P<0.05). The T-bilirubin and hs-CRP concentrations showed no difference among the groups, whereas the markers at 100 km were higher than those of the control and at 50 km (P<0.05). In conclusion, this study shows that the ultra-marathon race (100 km) may induce the damage of the skeletal muscle, liver and kidney, intravascular hemolysis and inflammatory responses.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.29 no.6
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• pp.828-836
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• 1996

The histological changes of gill, liver, spleen and muscle, and respiration and blood variables and liver glycogen content were examined in black seabream, Acanthopagrus schlegeli. Fish were exposed to a high level of total ammonia nitrogen (10.4 mg/l) and recovered from exposure $(0.4{\pm}0.2mg/l)$ in a closed recirculating seawater system. In the process of exposure, mortality was $9\%$, and hyperplasia, necrosis or inflammation appeared in all tissues except for muscle. Oxygen consumption was decreased by $49\%$, and red blood cell (RBC) number, hematocrit and hemoglobin concentration were significantly decreased, while plasma glucose contents, activities of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) increased. Liver glycogen content significantly increased from $6.6\%\;to\;10.4\%$. A large amount of hemosiderin was observed in the splenic tissue. During the recovery period, RBC number, hematocrit, hemoglobin concentration, GOT and GPT activities were returned to the normal status. Histological status of liver tissue was returned to the normal, but liver glycogen content was not recovered. During the recovery period, spleen melanin-macrophages temporarily increased, but subsequently decreased to the normal status.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2021.04a
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• pp.5-5
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• 2021

Alcoholic and nonalcoholic steaohepatitis is a leading form of chronic liver disease with few biomakers ad treatment options currently available. a progressive disease of NAFLD may lead to fibrosis, cirrhosis, and hepatocellular carcinoma. Recently, we extracted HIMH0021, which is an active flavonoid component in the Acer tegmentosum extract, has been shown to protect against liver damage caused by hepatic dysfunction. Therefore, in this study, we aimed to investigate whether HIMH0021 could regulate steatohepatitis and liver fibrosis during alcoholic or nonalcoholic metabolic process. HIMH0021, which was isolated from the active methanol extract of A. tegmentosum, inhibited alcohol-induced steatosis and attenuated the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) during hepatocellular alcohol metabolism, both of which promote lipogenesis as well as liver inflammation. Treatment with HIMH0021 conferred protection against lipogenesis and liver injury, inhibited the expression of cytochrome P4502E1, and increased serum adiponectin levels in the mice subjected to chronic-plus-binge feeding. Furthermore, in hepatocytes, HIMH0021 activated fatty acid oxidation by activating pAMPK, which comprises pACC and CPT1a. These findings suggested that HIMH0021 could be used to target a TNFα-related pathway for treating patients with alcoholic hepatitis.

• Korean Journal of Radiology
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• v.1 no.2
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• pp.98-103
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• 2000

Objective: The purpose of this study was to describe the CT findings of hepatic hypereosinophilic syndrome in which hepatic lobes or segments were involved. Materials and Methods: Seven patients with hypereosinophilic syndrome with hepatic lobar or segmental involvement were included in our study. In all seven, diagnosis was based on liver biopsy and the results of corticosteroid treatment. CT findings were retrospectively reviewed by three radiologists, who reached a consensus. Biopsy specimens were examined, with special reference to portal and periportal inflammation. Results: CT demonstrated well-defined, homogeneous or heterogeneous low attenuation with a straight margin limited to a hepatic lobe (n = 2), segments (n = 3), or subsegments (n = 2), particularly during the portal phase. Where there was subsegmental involvement, lesions were multiple, ovoid or wedge-shaped, and showed low attenuation. In two patients with lobar or segmental involvement, segmental portal vein narrowing was observed. Histopathologic examination disclosed eosinophilic infiltration in the periportal area, sinusoids and central veins, as well as portal phlebitis. Conclusion: Hypereosinophilic syndrome may involve the presence of hepatic lobar, segmental, or subsegmental low-attenuated lesions, as seen on CT images. Their presence may be related to damage of the liver parenchyma and to portal phlebitis.

• Journal of Life Science
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• v.19 no.10
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• pp.1360-1367
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• 2009

Liver fibrosis is a process of healing and scarring in response to chronic liver injury. Following injury, an acute inflammation response takes place resulting in moderate cell necrosis and extracellular matrix damage. To develop a novel therapeutic approach in hepatic fibrogenesis, we examined the simultaneous suppression of the transcription factors NF-$\kappa$B and Sp1, which regulate acute inflammation and continuous deposition of extracellular matrix in liver fibrosis. We employed chimeric decoy oligodeoxynucleotide containing the consensus sequences of both NF-$\kappa$B and Sp1 binding sites, to suppress these transcription factors simultaneously. Treatment of chimeric decoy oligodeoxynucleotide reduced the activity of hepatic stellate cells in vitro, and decreased the expression of fibrotic and proinflammatory gene responses in a mouse model of liver fibrosis. These results suggest that chimeric decoy oligodeoxynucleotide strategy can be a potential therapeutic application to prevent liver fibrosis.

• The Korea Journal of Herbology
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• v.33 no.1
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• pp.37-46
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• 2018

Objectives : Liver disease is an inflammatory reaction caused by oxidative stress, viral, alcohol, and drug properties. Inflammatory reaction causes hepatitis and chronic hepatitis is persistent, it progresses to liver fibrogenesis and liver cancer. The aim of this study was to confirm the hepatoprotective effect of Tongyuhwalhyeol-tang(Tongqiaohuoxue Decoction) (TH) and Gamtongyuhawlhyeol-tang(GTH) in TAA-induced liver injury animal model. Methods : The antioxidant activities were evaluated through in vitro experiments, such as 1, 1-diphenyl-2-picrylhydrazyl (DPPH) and 2, 2'-azinobis-3-ethyl-benzothiazoline-6-sulfonic acid (ABTS) radical scavenging assays, total polyphenol and total flavonoid content measurement. To confirm the liver protective effect, induced by Thioacetamide (TAA) for 3 days injection at 200 mg/kg rats. TH and GTH were treated 3 days at 200 mg/kg/day. The changes of reactive oxygen species (ROS), peroxynitrite ($ONOO^-$), alanine aminotransferanse (ALT) and aspartate aminotransferase (AST) in serum were analyzed after experiment. Also, expression of anti-inflammation, anti-oxidant related proteins were investigated by western blot analysis. Results : TH was inhibited the antioxidant activities. In the TAA-induced rat, TH decreased ROS, $ONOO^-$, ALT, AST level in serum. Inflammation related protein expressions increased in TAA-induced rat compared to normal rat. However, TH group inhibited the down expression of these proteins. Also, anti-oxidant related protein expressions increased in TH group compared TAA-induced rat. Conclusion : Therefor, these results suggested that TH provided hepatoprotective effects on the hepatic injury leading to the reduction of inflammatory response. In addition, the effect of TH was superior to that of GTH.

• Exercise Science
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• v.26 no.3
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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.

• Journal of Ginseng Research
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• v.43 no.2
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• pp.196-208
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• 2019

Background: Nonalcoholic steatohepatitis (NASH) is one of the chronic inflammatory liver diseases and a leading cause of advanced liver fibrosis, cirrhosis, and hepatocellular carcinoma. The main purpose of this study was to clarify the effects of GBCK25 fermented by Saccharomyces servazzii GB-07 and pectinase, on NASH severity in mice. Methods: Six-wk-old male mice were fed either a normal diet (ND) or a Western diet (WD) for 12 wks to induce NASH. Each group was orally administered with vehicle or GBCK25 once daily at a dose of 10 mg/kg, 20 mg/kg, 100 mg/kg, 200 mg/kg, or 400 mg/kg during that time. The effects of GBCK25 on cellular damage and inflammation were determined by in vitro experiments. Results: Histopathologic analysis and hepatic/serum biochemical levels revealed that WD-fed mice showed severe steatosis and liver injury compared to ND-fed mice. Such lesions were significantly decreased in the livers of WD-fed mice with GBCK25 administration. Consistently, mRNA expression levels of NASH-related inflammatory-, fibrogenic-, and lipid metabolism-related genes were decreased in the livers of WD-fed mice administered with GBCK25 compared to WD-fed mice. Western blot analysis revealed decreased protein levels of cytochrome P450 2E1 (CYP2E1) with concomitantly reduced activation of c-Jun N-terminal kinase (JNK) in the livers of WD-fed mice administered with GBCK25. Also, decreased cellular damage and inflammation were observed in alpha mouse liver 12 (AML12) cells and RAW264.7 cells, respectively. Conclusion: Administration of GBCK25 ameliorates NASH severity through the modulation of CYP2E1 and its associated JNK-mediated cellular damage. GBCK25 could be a potentially effective prophylactic strategy to prevent metabolic diseases including NASH.