• The Korean Journal of Physiology and Pharmacology
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• 제1권1호
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• pp.71-78
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• 1997

In an attempt to investigate the role of phospholipase $A_2$($PLA_2$) in interleukin-l (IL-l) induced acute lung injury, mepacrine was tried to inhibit $PLA_2$ in IL-l induced ARDS rats. For confirmation of acute lung injury by IL-l, and to know the role of neutrophils in this injury, lung leak index, lung myeloperoxidase(MPO), number of neutrophils and protein content in the bronchoalveolar lavage (BAL) and wet lung weight were measured. At the same time lung $PLA_2$ was measured to know the effect of IL-l on $PLA_2$ activity. Pulmonary surfactant was also measured for an investigation of type II alveolar cell function. Neutrophil adhesion assay was performed to know the effect of $PLA_2$ inhibition in vitro with human umbilical vein endothelial cells (HUVEC). For precise location of injury by IL-l, morpholgical study was performed by electron microscopy. Five hours after instillation of IL-l (50 ng/rat), lung leak index, protein content, number of neutrophils, lung MPO and wet lung weight were increased significantly. Five hours after IL-l instillation lung $PLA_2$ activity was increased significantly, and increased surfactant release was observed in IL-l induced ARDS rats' BAL. In contrast, in rats given mepacrine and IL-l, there was decrease of acute lung injury i.e. decrease of lung leak index, wet lung weight, protein content, number of neutrophils in BAL and decreased lung MPO activity. Mepacrine decreased surfactant release also. Interestingly, inhibition of $PLA_2$ decreased adhesion of human neutrophils to HUVEC in vitro. Morphologically, IL-l caused diffuse necrosis of endothelial cells, type I and II epithelial cells and increased the infiltration of neutrophils in the interstitium of the lung but after mepacrine treatment these pathological findings were lessened. On the basis of these experimental results it is suggested that $PLA_2$ has a major role in the pathogenesis of acute lung injury mediated by neutrophil dependent manner in IL-l induced acute lung injury.

• 대한한의학회지
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• 제23권3호
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• pp.174-187
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• 2002

Objectives : This study was carried out to determine whether Kamihaengche-tang plus Yulanijihwang-tang (KCYH) exerts a protective effect against oxidant-induced liver cell injury. Methods : Cell injury was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. Results : Oxidants (tBHP and $H_2O_2$) increased dose-dependently LDH release which was significantly prevented by 1% KCYH. The protective effect of KCYH against oxidant-induced cell injury was dose-dependent in the range of 0.05-1 % concentrations. Similarly, KCYH inhibited oxidant-induced lipid peroxidation in a dose-dependent manner. When liver tissues were exposed to Hg (0.5 mM), ALT activity in the medium and lipid peroxidation in tissues were markedly increased. These changes were prevented by 1% KCYH, KCYH restored toxicant-induced inhibition of cellular GSH content. KCYH increased the activities of catalase and glutathion peroxidase in oxidant-treated tissues. Conclusions : These results indicate that KCYH exerts a protective effect against oxidant-induced liver cell injury, and this effect is attributed to prevention of lipid peroxidation. These effects may be due to an increase in concentration of endogenous antioxidants.

• 생명과학회지
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• 제8권4호
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• pp.464-471
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• 1998

This study was carried out to determine whether Kamihaengche-tang plus Yukmijihwang-tang (KCYH) exerts the protective effect against oxidant-induced liver cell injury. Cell injurt was estimated by measuring lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) release, and lipid peroxidation was estimated by measuring malondialdehyde, a product of lipid peroxidation in rabbit liver slices. $H_2O_2$increased LDH release which was significantly prevented by 1% KCYHT. The protective effect of KCYH against $H_2O_2$-induced cell injury was dose-dependent in the range of 0.05-1% concentrations. Similary, KCYH inhibited $H_2O_2$ induced lipid peroxidation in a dose-dependent manner. When liver tissuse were exposed to Hg(0.5 mM), ALT activity in the medium and lipid erpoxidation in tissues were markedly increased. These changes were prevented by 1% KCYH. KCHY restored Hg-induced inhibition of cellular GSH content. These result indicate that KCYH exerts the protective effect oxidant-induced liver cell injury, and this effect is attributed to prevented to prevention of lipid peroxidation. These dffects may be due to an increase in concentration of endogenous antioxidants.

• 사상체질의학회지
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• 제22권2호
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• pp.135-142
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• 2010

1. Objectives: The purpose of this case is to report that a Tae-eumin patient diagnosed as drug-induced liver injury (DILI) caused by Galgeunhaegi-tang (Gegenjieji-tang) treated with Taeumjowe-tang reduced ephedra to 2g (Taiyintiaowei-tang) and then liver function test Results: improved. 2. Methods: We diagnosed him as Tae-eumin Exterior cold disease induced from the esophagus affected by cold. We made him stop taking Galgeunhaegi-tang (Gegenjieji-tang) and take Taeumjowe-tang reduced ephedra to 2g. (Taiyintiaowei-tang) 3. Results: After our treatment, the symptom and the liver function test Results: improved. 4. Conclusions: The wrong diagnosis of constitution and pathological syndromes can be caused drug-induced liver injury. Taeumjowe-tang reduced ephedra to 2g (Taiyintiaowei-tang) may have an effect on treatment of drug-induced liver injury of Tae- eumin.

• Biomolecules & Therapeutics
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• 제25권4호
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• pp.367-373
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• 2017

This study was performed to evaluate whether microRNAs (miRNAs) in circulating exosomes may serve as biomarkers of drug-induced liver, kidney, or muscle-injury. Quantitative PCR analyses were performed to measure the amounts of liver-specific miRNAs (miR-122, miR-192, and miR-155), kidney-specific miR-146a, or muscle-specific miR-206 in plasma and exosomes from mice treated with liver, kidney or muscle toxicants. The levels of liver-specific miRNAs in circulating plasma and exosomes were elevated in acetaminophen-induced liver injury and returned to basal levels by treatment with antioxidant N-acetyl-cysteine. Circulating miR-146a and miR-206 were increased in cisplatin-induced nephrotoxicity and bupivacaine-induced myotoxicity, respectively. Taken together, these results indicate that circulating plasma and exosomal miRNAs can be used as potential biomarkers specific for drug-induced liver, kidney or muscle injury.

• 한국미생물·생명공학회지
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• 제50권1호
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• pp.157-163
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• 2022

Alcoholic liver disease (ALD), which encompasses alcoholic steatosis, alcoholic hepatitis, and alcoholic cirrhosis, is a major cause of morbidity and mortality worldwide. Although the economic and health impacts of ALD are clear, few advances have been made in its prevention or treatment. We recently demonstrated that the insect-derived antimicrobial peptide CopA3 exerts anti-apoptotic and anti-inflammatory activities in various cell systems, including neuronal cells and colonic epithelial cells. Here, we tested whether CopA3 inhibits ethanol-induced liver injury in mice. Mice were intraperitoneally injected with ethanol only or ethanol plus CopA3 for 24 h and then liver injury and inflammatory responses were measured. Ethanol enhanced the production of proinflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interferon (IFN)-γ, and IL-10. It also induced hepatocyte apoptosis and ballooning degeneration in hepatocytes. Notably, all these effects were eliminated or significantly reduced by CopA3 treatment. Collectively, our findings demonstrate that CopA3 ameliorates ethanol-induced liver cell damage and inflammation, suggesting the therapeutic potential of CopA3 for treating ethanol-induced liver injury.

• 대한의생명과학회지
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• 제11권4호
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• pp.441-446
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• 2005

The molecular mechanism of ischemia/reperfusion injury remains unclear. Reactive oxygen species (ROS) are implicated in cell death caused by ischemia/reperfusion in vivo or hypoxia in vitro. Poly (ADP-ribose) polymerase (PARP) activation has been reported to be involved in hydrogen peroxide-induced cell death in renal epithelial cells. This study was therefore undertaken to evaluate the role of P ARP activation in chemical hypoxia in opossum kidney (OK) cells. Chemical hypoxia was induced by incubating cells with antimycin A, an inhibitor of mitochondrial electron transport. Exposure of OK cells to chemical hypoxia resulted in a time-dependent cell death. In OK cells subjected to chemical hypoxia, the generation of ROS was increased, and this increase was prevented by the $H_2O_2$ scavenger catalase. Chemical hypoxia increased P ARP activity and chemical hypoxia-induced cell death was prevented by the inhibitor of PARP activation 3-aminobenzamide. Catalase prevented OK cell death induced by chemical hypoxia. $H_2O_2$ caused PARP activation and $H_2O_2-induced$ cell death was prevented by 3-aminobenzamide. Taken together, these results indicate that chemical hypoxia-induced cell injury is mediated by PARP activation through H202 generation in renal epithelial cells.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제21권4호
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• pp.347-350
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• 2018

Drug-induced autoimmune hepatitis (DIAIH) is an increasingly recognized form of drug-induced liver injury that leads to a condition similar to idiopathic autoimmune hepatitis. A number of drugs have been associated with DIAIH, minocycline is one of the most well characterized. Minocycline is a semisynthetic tetracycline antibiotic used in the treatment of acne vulgaris. Minocycline-induced autoimmune hepatitis presents with serologic and histologic features similar to idiopathic autoimmune hepatitis. However, the natural history and outcomes of these two conditions differ significantly. The majority of patients with minocycline-induced autoimmune hepatitis experience complete resolution of symptoms after withdrawal of the medication. Some patients may require a short course of steroids and rarely use of an immunomodulator to achieve resolution of disease. Recurrence of symptoms is rare and typically only occurs with reintroduction of minocycline. It is important for primary care providers to consider minocycline-induced autoimmune hepatitis when liver injury develops during minocycline therapy.

• Journal of Acupuncture Research
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• 제26권5호
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• pp.85-94
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• 2009

Objectives : This study was designed to investigate the effect of pharmacopuncture of Mori Cortex on galactosamine-induced liver injury in rats. Methods : Male Sprague-Dawley rats were divided into 5 groups; Normal, liver injury not induced and not treated group. Control, the liver injury-induced and not treated group. Saline group, the liver injury-induced and saline injection at $BL_{18}$. HA-1 and HA-2 group, the liver injury-induced and pharmacopuncture of Mori Cortex applied to $BL_{18}$, each $1.3{\mu}g/g$, $2.6{\mu}g/g$. Then we observed the changes of ${\gamma}$-GTP, GOT, GPT, LDH, total cholesterol, triglyceride, total bilirubin. Results : Pharmacopuncture of Mori Cortex treatment significantly inhibited the activities of ${\gamma}$-GTP, GOT, total cholesterol, triglyceride and total bilirubin in HA-1 group. ${\gamma}$-GTP, GTP, LDH, ${\gamma}$-GTP levels were significantly inhibited in HA-2 group. Conclusions : These results demonstrate that the reduce of hepatic enzyme activation and lipid accumulation by pharmacopuncture of Mori Cortex may be by an antioxidant properties of Mori Cortex.

• 대한한방내과학회지
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• 제40권6호
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• pp.1035-1042
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• 2019

Background: Herbal medication is widely used in the Korean Medicine Hospital, and drug-induced liver injury (DILI) in Korea has increased proportionally. Herb-induced liver injury now accounts for approximately 40% of cases of hepatotoxicity in Korea, according to research data. Currently, however, the component responsible for the toxicity is usually unknown or can only be suspected. Objective: To study the hepatotoxicity of Cheongsimyeonja-tang in DILI. Methods: A retrospective review was conducted of 82 inpatients between April 2010 and March 2017 with suspected drug-induced liver injury (n=5). The standard criteria (RUCAM scale) for drug-induced liver injury (DILI) were applied. The electronic medical records (EMRs) were retrospectively reviewed to identify the relevant database. Aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin (T. Bili) were analyzed in blood samples before and after the administration of Cheongsimyeonja-tang. Results: Five cases out of 82 patients had a criterion-referenced probable (RUCAM) score ranging from 6 to 8 points DILI. However, statistical analysis of the liver function parameters results of the 82 patients did not show a statistically meaningful elevation after taking Cheongsimyeonja-tang. Conclusions: These data suggest a relationship between Cheongsimyeonja-tang and DILI. More studies are needed to validate these observations and to explore their implications.