• 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.

• Nutritional Sciences
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• v.9 no.2
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• pp.106-111
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• 2006

Chronic alcohol consumption is associated with perturbation of hepatic metabolism of sulphur-containing amino acid. The goal of present study was to evaluate the influence of dietary supplementation of methionine or folate to chronically ethanol-fed mts on the metabolism of sulfur-containing amino acids and one-carbon metabolism. Sprague-Dawley male mts were fed Lieber-Decarli liquid diet with 0% ethanol (control), 36% ethanol (E), 36% ethanol combined with methionine supplement (EM) or folate supplement (EF) for 8 weeks. Hepatic S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), plasma folate and homocysteine (Hcy), urinary excretion of folate and formiminoglutamate were investigated after feeding experimental diets. Growth was retarded by 36% ethanol consupmtion (E, EM and EF) (p<0.01). Liver total fat (p<0.05) and plasma ALT (P<0.01) were increased by methionine supplementation (EM), implicating fatty liver and liver injury. Liver folate was increased slightly by folate supplementation (EF) (p=0.077). Urinary folate loss was increased 2.3 fold by ethanol consumption (E) and 17.2 fold by folate supplementation (EF), while decreased by methionine supplementation (EM) (p<0.000l). Plasma Hcy was increased 1.9 fold by methionine supplementation (EM) in ethanol-fed mts (p<0.05), which was related with decreased methionine synthase activity (p<0.05). Hepatic SAM/SAH ratio was depressed by methionine supplementation in ethanol-fed mts (EM) (p<0.05). Urinary formininoglutamate (Figlu) excretion after histidine loading was increased by ethanol ingestion and reduced by methionine supplementation (p<0.00l). Based on these data, methionine supplementation appears to accelerate histidine oxidation. In conclusion, dietary supplementation of methionine to ethanol-fed mts exacerbates alcoholic liver injury possibly by complicating sulphur-containing amino acid metabolism, as while it may have beneficial effects on folate and histidine metabolism.

• Journal of Microbiology and Biotechnology
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• v.34 no.3
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• pp.606-621
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• 2024

This study evaluated the hepatoprotective effect of fermented Protaetia brevitarsis larvae (FPB) in ethanol-induced liver injury mice. As a result of amino acids in FPB, 18 types of amino acids including essential amino acids were identified. In the results of in vitro tests, FPB increased alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) activities. In addition, FPB treatment increased cell viability on ethanol- and H₂O₂-induced HepG2 cells. FPB ameliorated serum biomarkers related to hepatoxicity including glutamic oxaloacetic transaminase, glutamine pyruvic transaminase, total bilirubin, and lactate dehydrogenase and lipid metabolism including triglyceride, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Also, FPB controlled ethanol metabolism enzymes by regulating the protein expression levels of ADH, ALDH, and cytochrome P450 2E1 in liver tissue. FPB protected hepatic oxidative stress by improving malondialdehyde content, reduced glutathione, and superoxide dismutase levels. In addition, FPB reversed mitochondrial dysfunction by regulating reactive oxygen species production, mitochondrial membrane potential, and ATP levels. FPB protected ethanol-induced apoptosis, fatty liver, and hepatic inflammation through p-AMP-activated protein kinase and TLR-4/NF-κB signaling pathways. Furthermore, FPB prevented hepatic fibrosis by decreasing TGF-β1/Smad pathway. In summary, these results suggest that FPB might be a potential prophylactic agent for the treatment of alcoholic liver disease via preventing liver injury such as fatty liver, hepatic inflammation due to chronic ethanol-induced oxidative stress.

• Journal of Environmental Health Sciences
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• v.23 no.1
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• pp.81-94
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• 1997

The concentrations of cadmium, metallothionein(MT), superoxide dismutase(SOD), and lactate dehydrogenase(LDH) were investigated in liver and kidney of rats which were fed the water containing 50 or 100ppm cadmium chloride with basal diet(group A), 5% horsetail diet(group, B), 5% mugwort diet(group C) and 5% champignon diet(group D) for weeks. Cadmium in liver decreased for the first 12 weeks of treatment, but thereafter increased, and was lower in experimental group B,C,D than in control group A. Cadmium in kidney increased linearly during the 16 weeks of treatment, and was lower in group B than in group A. MT in liver decreased for the first 12 weeks of treatment in group A, but increased linearly during the 16 weeks in group B,C,D, higher in group B than in group A. There were significantly higher accumulation of cadmium and MT in liver than in kidney in the beginning of cadmium treatment, but reversed in the ending of treatment. The SOD and LDH activities were not affected during the 16 weeks treatment, and there was no significant difference between groups. Histologic examination revealed moderate to severe hepatic and renal injury in group A compared to horsetail diet group B. These results indicate that the kidney is a major target organ of chronic cadmium poisoning, and suggest that Cd-induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity. In addition, higher MT concentrations in liver and kidney in the group B constitute a plausible explanation of the protective effects of horsetail diet against the cadmium toxicity in relation to histologic findings.

• Molecules and Cells
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• v.41 no.5
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• pp.401-412
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• 2018

Oxymatrine (OMT) often used in treatment for chronic hepatitis B virus infection in clinic. However, OMT-induced liver injury has been reported. In this study, we aim to investigate the possible mechanism of OMT-induced hepatotoxicity in human normal liver cells (L02). Exposed cells to OMT, the cell viability was decreased and apoptosis rate increased, the intracellular markers of oxidative stress were changed. Simultaneously, OMT altered apoptotic related proteins levels, including Bcl-2, Bax and pro-caspase-8/-9/-3. In addition, OMT enhanced the protein levels of endoplasmic reticulum (ER) stress makers (GRP78/Bip, CHOP, and cleaved-Caspase-4) and phosphorylation of c-Jun N-terminal kinase (p-JNK), as well as the mRNA levels of GRP78/Bip, CHOP, caspase-4, and ER stress sensors (IREI, ATF6, and PERK). Pre-treatment with Z-VAD-fmk, JNK inhibitor SP600125 and N-acetyl-l-cysteine (NAC), a ROS scavenger, partly improved the survival rates and restored OMT-induced cellular damage, and reduced caspase-3 cleavage. SP600125 or NAC reduced OMT-induced p-JNK and NAC significantly lowered caspase-4. Furthermore, 4-PBA, the ER stress inhibitor, weakened inhibitory effect of OMT on cells, on the contrary, TM worsen. 4-PBA also reduced the levels of p-JNK and cleaved-caspase-3 proteins. Therefore, OMT-induced injury in L02 cells was related to ROS mediated p-JNK and ER stress induction. Antioxidant, by inhibition of p-JNK or ER stress, may be a feasible method to alleviate OMT-induced liver injury.

• Journal of Applied Biological Chemistry
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• v.59 no.3
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• pp.265-271
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• 2016

Recently, liver damage contributes to big percentage of the morbidity and mortality rates worldwide. Excessive intake of alcohol is one of the major causes of liver injury. When liver injury is repeated and becomes chronic, it leads to development of fibrosis and cirrhosis. In the liver, TGF-${\beta}$ is a profibrogenic cytokine, which participates in various critical events cause liver fibrosis. Seahorse (Hippocampus abdominalis) is a common traditional Chinese medicine and has been widely used for centuries. Seahorse has been known to have a variety of bioactivities, such as anti-oxidant, anti-fatigue, and anti-tumor. Peptide is one of the main compounds of seahorse. In this study, we isolated enzymatic hydrolysate from seahorse H. abdominalis by alcalase hydrolysis and investigated the effect of the hydrolysate on liver injury. In the present in vitro studies, the hydrolysate increases cell viability of Chang cells and protects Huh7 cells from ethanol toxicity. In addition, the hydrolysate inhibits TGF-${\beta}$-induced responses. In vivo studies show that the pretreatment of hydrolysate reduces alcohol-induced increases of serum Glutamic oxaloacetic acid transaminase and Glutamic pyruvate transaminase activities and increases liver weight and body weight. These results suggest that seahorse may have a hepatoprotective effect.

• Laboraroty Animal Research
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• v.34 no.4
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• pp.133-139
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• 2018

Nonalcoholic steatohepatitis (NASH) is becoming common chronic liver disease because of the increasing global prevalence of obesity and consequently Nonalcoholic fatty liver disease (NAFLD). However, the mechanism for progression of NAFLD to NASH and then cirrhosis is not completely understood, yet. The triggering of these hepatic diseases is thought from hepatocyte injury caused by over-accumulated lipid toxicity. Injured hepatocytes release damage-associated molecular patterns (DAMPs), which can stimulate the Kupffer cells (KCs), liver-resident macrophages, to release pro-inflammatory cytokines and chemokines, and recruit monocyte-derived macrophages (MDMs). The increased activation of KCs and recruitment of MDMs accelerate the progression of NAFLD to NASH and cirrhosis. Therefore, characterization for activation of hepatic macrophages, both KCs and MDMs, is a baseline to figure out the progression of hepatic diseases. The purpose of this review is to discuss the current understanding of mechanisms of NAFLD and NASH, mainly focusing on characterization and function of hepatic macrophages and suggests the regulators of hepatic macrophages as the therapeutic target in hepatic diseases.

• Journal of Trauma and Injury
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• v.32 no.1
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• pp.66-70
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• 2019

Traumatic diaphragmatic injuries (TDIs) are a rare complication in thoraco-abdominal trauma. The diagnosis is difficult and if left untreated, TDI can cause traumatic diaphragmatic hernia (TDH). Through an injured diaphragm, the liver, spleen, stomach, small intestine, and large intestine can be herniated to the thoracic cavity, but pancreatic herniation and pancreatitis are quite rare in TDH. This paper reports a case of pancreatitis developed by additional trauma in a patient with asymptomatic chronic TDH. A 58-year-old male visited the emergency department with a left abdominal injury after a fall 6 hours earlier. The vital signs were stable, but the amylase and lipase levels were elevated to 558 U/L and 1,664 U/L, respectively. Abdominal computed tomography (CT) revealed a left diaphragmatic hernia and an incarceration of the stomach, pancreatic ductal dilatation, and peripancreatic fatty infiltration. Additional history taking showed that he had suffered a fall approximately 20 years ago and had an accidentally diaphragmatic hernia through a chest CT 6 months earlier. A comparison with the previous CT revealed the pancreatitis to be caused by secondary pancreatic ductal obstruction due to the incarcerated stomach. For pancreatitis, gastrointestinal decompression was performed, and after 3 days, the pancreatic enzyme was normalized; hence, a thoracotomy was performed. A small ruptured diaphragm was found and reposition of the organs was performed. This paper reports the experience of successfully treating pancreatitis and pancreatic hernia developed after trauma without complications through a thoracotomy following gastrointestinal decompression.

• Journal of radiological science and technology
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• v.12 no.1
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• pp.3-16
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• 1989

In order to investigate the in vivo effect of $^{60}Co$ radiation on rabbit liver, the uptake ratio and regional excretory value in hepatocytes and Kupffer cells were estimated during acute and chronic hepatic injuries. The left lobe of liver was irradiated at 15 Gy or 30 Gy with a single dose and subsequent changes were analysed with a seial nuclear medicine imaging by using $^{99m}Tc-phytate,\;^{99m}Tc-DISIDA\;and\;^{99m}Tc-HSA$ and resulting data were computerized. The degree of hepatic damage, duration of the injury, and recovery pattern after the irradation were in agreement with the findings of other investigations. However, out values were more quantitative evacuation than those of other publications. Recovery of decreased uptake of $^{99m}Tc-phytate$ was delayed approximately $2{\sim}3$ days later than that of $^{99m}Tc-DISIDA$. In acute radiation induced injury, the results demonstrated that the recovery of Kupffer cells was delayed more than that of hepatocytes. This discrepancy was considered due to the differences in repair activities between these cell types. The decreased of regional excretory value in irradiated area was found to be dose-dependent but had no corelation with regional uptakes of DISIDA and phytate. The decreased of regional excretory value observed in non-irradiated region suggested that irradiated liver might induce an indirect effect.

• Journal of Acupuncture Research
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• v.25 no.4
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• pp.117-125
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• 2008

Objectives : Analyze according to types of event causing the adverse outcome due to acupotomy, and discuss problems and safety reqirements to using this therapy in Korea. Methods : Based upon the indication, contraindication, treatment procedures, clinical obsevations, acupotomy-related adverse outcome case reports, the factors of damaging event were classified. Results : The main factors of adverse outcome by acupotomy were anatomical ignorance, contamination of device or hospital staff, failure to notice preexisting disease(cardiovascular disease, hypertension, renal failure, hemophilia, chronic Liver Disease, etc.), unskilled treatment procedures(massive bleeding) and techniques(nerve injury, hepatic and splenic injury, Pneumothorax). Conclusions : It is mandatory to prepare adequate sterilie aseptic technique. The clinician should ensure understand genernal health state of patient and anatomical direction.