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Daram Yang,Hyuneui Jeong,Seung-Mi Hwang,Jong-Won Kim,Hee-Won Moon,Ye-Eun Lee,Hyo-Bin Oh,Chung-berm Park,Bumseok Kim 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.1
Background: Nonalcoholic steatohepatitis (NASH) is one of the main chronic liver diseases. NASH is identified by lipid accumulation, inflammation, and fibrosis. Jinan Red Ginseng (JRG) and licorice have been widely used because of their anti-inflammatory and hepatoprotective effects. Hence, this study assessed JRG and licorice extract mixtures" effects on NASH progression. Methods: Palmitic acid (PA) and the western diet (WD) plus, high glucose-fructose water were used to induce in vitro and in vivo NASH. Mice were orally administered with JRG-single (JRG-S) and JRG-mixtures (JRG-M; JRG-S + licorice) at 0, 50, 100, 200 or 400 mg/kg/day once a day during the last half-period of diet feeding. Results: JRG-S and JRG-M reduced NASH-related pathologies in WD-fed mice. JRG-S and JRG-M consistently decreased the mRNA level of genes related with inflammation, fibrosis, and lipid metabolism. The treatment of JRG-S and JRG-M also diminished the SREBP-1c protein levels and the p-AMPK/AMPK ratio. The FAS protein levels were decreased by JRG-M treatment both in vivo and in vitro but not JRG-S. Conclusion: JRG-M effectively reduced lipogenesis by modulating AMPK downstream signaling. Our findings suggest that this mixture can be used as a prophylactic or therapeutic alternative for the remedy of NASH.
Fabrication of the Superhydrophobic Surface Inspired from Lotus-Effect
Dae-Hwan Jung(정대환),Hyuneui Lim(임현의),Jeong-Hyun Noh(노정현),Wan-Doo Kim(김완두) 대한기계학회 2007 대한기계학회 춘추학술대회 Vol.2007 No.5
Wettability of solid surfaces with liquids is governed by the chemical properties and the microstructure of the surfaces. We report on the preparation of liquid-repellent surfaces using surface-attached monolayers of perfluorinated polymer molecules on porous silica substrates. A covalent attachment of the polymer molecules to the substrate is achieved by generation of the polymer chains through starting a surface-initiated radical-chain polymerization of a fluorinated monomer. To this, self-assembled monolayers of azo initiators are attached to silica substrates, which are used to kick off the polymerization reaction in situ. The growth of the fluorinated polymer films and the characterization of the obtained surfaces by surface plasmon spectroscopy, XPS, and contact angle measurements is described. It is shown that perfluorinated polymer films can be grown with controlled thicknesses on flat and even on porous silica surfaces, essentially without changing the surface roughness. The combination of the low surface energy coating and the surface porosity allows generation of materials which are both water and oil repellent.
Yang Daram,Kim Jong Won,Jeong Hyuneui,Kim Min Seok,Lim Chae Woong,Lee Kyuhong,Kim Bumseok 한국독성학회 2023 Toxicological Research Vol.39 No.1
Cigarette smoke (CS) is a dominant carcinogenic agent in a variety of human cancers. CS exposure during pregnancy can adversely affect the fetus. Non-alcoholic fatty liver disease (NAFLD) is considered as a hepatic manifestation of a metabolic disorder, and ranges from simple steatosis to cirrhosis leading to hepatocellular carcinoma. Non-alcoholic steatohepatitis (NASH) is a more severe phase of NAFLD. Recently, there is increasing apprehension about the CS-related chronic liver diseases. Therefore, we examined whether maternal CS exposure could affect the pathogenesis of NASH in offspring. Mainstream CS (MSCS) was exposed to pregnant C57BL/6 mice via nose-only inhalation for 2 h/day, 5 days/week for 2 weeks from day 6 to 17 of gestation at 0, 300, or 600 μg/L. Three-week-old male offspring mice were fed methionine and cholinesupplemented (MCS) diet or methionine and choline-deficient including high-fat (MCDHF) diet for 6 weeks to induce NASH. Maternal MSCS exposure increased the severity of NASH by increasing serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, hepatic total cholesterol (TC) and triglyceride (TG) levels, pro-inflammation, fibrosis, and steatosis in offspring mice. Especially, maternal MSCS exposure significantly downregulated the phosphorylation of AMPactivated protein kinase (AMPK) in MCDHF diet-fed offspring mice. Subsequently, the protein levels of sterol regulatory element-binding protein (SREBP)-1c and stearoyl-CoA desaturase-1 (SCD1) were upregulated by maternal MSCS exposure. In conclusion, maternal MSCS exposure exacerbates the progression of NASH by modulating lipogenesis on offspring mice.
Γ-Aminobutyric acid promotes methionine-choline deficient diet-induced nonalcoholic steatohepatitis
Seok Roh, Yoon,Cho, Ara,Zhou, Zixiong,Jeong, Hyuneui,Park, Jeong-Eun,Cha, Youn-Soo,Oh, Suk-Heung,Lim, Chae-Woong,Kim, Bumseok Editorial Department of Journal of Biomedical Rese 2017 JOURNAL OF BIOMEDICAL RESEARCH -ELSEVIER- ENGLISH Vol.31 No.1
<P><B>Abstract</B></P><P>Nonalcoholic steatohepatitis (NASH) is one of the most common liver diseases and a major cause of liver fibrosis worldwide. Γ-Aminobutyric acid (GABA) is one of the most abundant inhibitory neurotransmitters in the central nervous system. Recently, it has been reported that GABAergic signaling pathways are found in various non-neuronal tissues including the immune system and play a functional role. In the present study, we investigated whether administration of GABA has effects on NASH through its immunomodulatory effects. To test this hypothesis, C57BL/6 mice were fed a methionine–choline-deficient (MCD) diet for 8 weeks. After four weeks into MCD feeding, mice were provided with plain water (control) or water containing 2 mg/mL of GABA for the subsequent 4 weeks. Using this MCD diet-induced NASH model, we found that mice receiving GABA showed more severe steatohepatitis and liver fibrosis than control mice. This increased liver damage was confirmed by higher levels of serum alanine transaminase (ALT) and aspartate aminotransferase (AST) compared to the control group. In accordance with increased liver steatohepatitis, NASH-related and inflammatory gene expression (collagen α1, tissue inhibitor of metalloproteinase-1, TNF-α) in the liver was markedly increased in GABA-treated mice. Furthermore, GABA directly enhanced production of inflammatory cytokines including IL-6 and TNF-α in LPS activated RAW macrophage cells and increased TIB–73 hepatocyte death. Such effects were abolished when GABA was treated with bicuculline, a competitive antagonist of GABA receptors. These results suggest that oral administration of GABA may be involved in changes of the liver immune milieu and conferred detrimental effects on NASH progression.</P>
Seo Yoon-Seok,Park Kwang-Hoon,Park Jung-Min,Jeong Hyuneui,Kim Bumseok,Jeon Jang Su,Yu Jieun,Kim Sang Kyum,Lee Kyuhong,Lee Moo-Yeol 한국독성학회 2024 Toxicological Research Vol.40 No.2
Smoking is a well-established risk factor for various pathologies, including pulmonary diseases, cardiovascular disorders, and cancers. The toxic effects of cigarette smoke (CS) are mediated through multiple pathways and diverse mechanisms. A key pathogenic factor is oxidative stress, primarily induced by excessive formation of reactive oxygen species. However, it remains unclear whether smoking directly induces systemic oxidative stress or if such stress is a secondary consequence. This study aimed to determine whether short-term inhalation exposure to CS induces oxidative stress in extrapulmonary organs in addition to the lung in a murine model. In the experiment, 3R4F reference cigarettes were used to generate CS, and 8-week-old male BALB/c mice were exposed to CS at a total particulate matter concentration of either 0 or 800 μg/L for four consecutive days. CS exposure led to an increase in neutrophils, eosinophils, and total cell counts in bronchoalveolar lavage fluid. It also elevated levels of lactate dehydrogenase and malondialdehyde (MDA), markers indicative of tissue damage and oxidative stress, respectively. Conversely, no significant changes were observed in systemic oxidative stress markers such as total oxidant scavenging capacity, MDA, glutathione (GSH), and the GSH/GSSG ratio in blood samples. In line with these findings, CS exposure elevated NADPH oxidase (NOX)-dependent superoxide generation in the lung but not in other organs like the liver, kidney, heart, aorta, and brain. Collectively, our results indicate that short-term exposure to CS induces inflammation and oxidative stress in the lung without significantly affecting oxidative stress in extrapulmonary organs under the current experimental conditions. NOX may play a role in these pulmonary-specific events.