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Yun Ho Jo,Hwan Lee,Myeong Hwan Oh,Gyeong Hee Lee,You Jin Lee,Ji Sun Lee,Min Jung Kim,Won Yong Kim,Jin Seong Kim,Dae Seok Yoo,Sang Won Cho,Seon Woo Cha,Mi Kyung Pyo 한국영양학회 2020 Nutrition Research and Practice Vol.14 No.4
BACKGROUND/OBJECTIVES: This study was designed to investigate the improvement effect of white ginseng extract (GS-KG9) on D-galactosamine (Ga1N)-induced oxidative stress and liver injury. SUBJECTS/METHODS: Sixty Sprague-Dawley rats were divided into 6 groups. Rats were orally administrated with GS-KG9 (300, 500, or 700 mg/kg) or silymarin (25 mg/kg) for 2 weeks. The rats of the GS-KG9- and silymarin-treated groups and a control group were then intraperitoneally injected Ga1N at a concentration of 650 mg/kg for 4 days. To investigate the protective effect of GS-KG9 against GalN-induced liver injury, blood liver function indicators, anti-oxidative stress indicators, and histopathological features were analyzed. RESULTS: Serum biochemical analysis indicated that GS-KG9 ameliorated the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in GalN-treated rats. The hepatoprotective effects of GS-KG9 involved enhancing components of the hepatic antioxidant defense system, including glutathione, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT). In addition, GS-KG9 treatment inhibited reactive oxygen species (ROS) production induced by GalN treatment in hepatocytes and significantly increased the expression levels of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) proteins, which are antioxidant proteins. In particular, by histological analyses bases on hematoxylin and eosin, Masson"s trichrome, α-smooth muscle actin, and transforming growth factor-β1 staining, we determined that the administration of 500 mg/kg GS-KG9 inhibited hepatic inflammation and fibrosis due to the excessive accumulation of collagen. CONCLUSIONS: These findings demonstrate that GS-KG9 improves GalN-induced liver inflammation, necrosis, and fibrosis by attenuating oxidative stress. Therefore, GS-KG9 may be considered a useful candidate in the development of a natural preventive agent against liver injury.
송성태(Sung Tae Song),최문규(Moon Kyu Choi),박상구(Sang Gu Park),장호환(Ho Hwan Jang),차효정(Hyo Jung Cha) 한국철도학회 2012 한국철도학회 학술발표대회논문집 Vol.2012 No.5
1992년 첫 삽을 뜨면서 시작한 경부고속철도건설사업이 2004년 4월, 1단계 개통을 한데 이어 지난 2010년 11월 완전 개통하였다. 경부고속철도 개통으로 경부축 지역의 2시간대 서비스 제공을 통한 국토의 균형발전 촉진 및 여가·관광사업 활성화, 기술발전, 환경비용 및 에너지 절감 등 긍정적인 효과를 이룬 반면, 잦은 기본계획 변경으로 인한 사업비 및 사업기간의 증가, 현실과 맞지 않은 설치기준으로 인한 과잉설계 문제 등 부정적 효과도 초래했다. 본 연구를 통해 사업추진 단계별 주요 이슈에 대해 객관적인 시각으로 문제점을 분석하고 시사점을 도출함으로써, 현재 추진하고 있는 호남고속철도와 수도권고속철도 사업에서는 시행착오를 줄이고 사업을 효율적으로 추진하는데 활용하고자 한다. Launched in 1992, the Gyeung-Bu High Speed Railway (HSR) was fully opened in November 2010 following the partial opening of the first phase in April 2004. Since the opening it has made tremendous achievements, including but not limited to, technical innovation, balanced regional development, growth of leisure and tourism industries, and savings of environmental costs and energy. On the other hand, it has brought negative effects such as increase in project time and cost by frequent changes of the basic plan and over-design based on unrealistic criteria. In this study we will analyze major issues that occurred at each stage of the Gyeong-Bu HSR project and draw implications. Thus, this study will enhance to efficiently implement the Ho-Nam and Seoul Metropolitan HSR project through minimizing possible trials and errors.
5kW급 계통연계형 단상 배터리 충전기의 구현 및 실험
안현성(Hyun-Sung An),이우종(Wujong Lee),문병호(Byung-Ho Mun),박일규(Il-Kyu Park),정선용(Seon-Yong Jung),김영록(Youngroc Kim),차한주(Hanju Cha1) 전력전자학회 2013 전력전자학회 논문지 Vol.18 No.1
This paper explains control methods of single-phase grid connected battery charger. Charging mode is control by Constant Current - Constant Voltage method and discharging mode is controlled by active-reactive power control method. Current control method is based on the synchronous reference frame(SRF) PI controller, and the second harmonic of battery current is compensated by an added L-C resonant circuit. Feasibility of the proposed control methods is verified through experiment with a prototype of 5kW single-phase grid connected battery charger.
Lee, Moon Hee,Cha, Hee-Jae,Choi, Eun Ok,Han, Min Ho,Kim, Sung Ok,Kim, Gi-Young,Hong, Su Hyun,Park, Cheol,Moon, Sung-Kwon,Jeong, Soon-Jeong,Jeong, Moon-Jin,Kim, Wun-Jae,Choi, Yung Hyun Spandidos Publications 2017 International journal of molecular medicine Vol.39 No.3
<P>Natural phytochemicals of plant origin, including flavonoids, have been found to be potent antioxidants providing beneficial effects against oxidative stress-related diseases. The present study was carried out to investigate the antioxidant properties of morin, a flavonoid originally isolated from the flowering plants of the Moraceae family. Superoxide dismutase (SOD)-like activity and 2,2'-azino-bis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS(center dot+)) radical scavenging activity were determined. We also investigated the cytoprotective effects of morin against hydrogen peroxide (H2O2)-induced DNA damage and apoptosis in V79-4 Chinese hamster lung fibroblasts. Our results demonstrated that morin had strong scavenging effects against ABTS' radicals with enhanced SOD activity, which varied in a dose-dependent manner. Morin was found to reduce H2O2-induced intracellular reactive oxygen species generation and nuclear DNA damage, and it recovered cell viability damaged by H2O2 via inhibition of mitochondrial dysfunction-mediated apoptosis. Notably, the treatment of V79-4 cells with morin markedly enhanced the expression of heme oxygenase-1 (HO-1) but not quinone oxidoreductase-1, which was associated with the increased expression and phosphorylation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and the downregulation of Kelch-like ECH-associated protein 1 expression. Based on our findings, we conclude that morin effectively ameliorated oxidative stress-induced DNA damage through intrinsic free radical scavenging activity and activation of the Nrf2/HO-1 pathway.</P>
Lee, Moon Hee,Han, Min Ho,Lee, Dae-Sung,Park, Cheol,Hong, Su-Hyun,Kim, Gi-Young,Hong, Sang Hoon,Song, Kyoung Seob,Choi, Il-Whan,Cha, Hee-Jae,Choi, Yung Hyun UNKNOWN 2017 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.39 No.2
<P>In the present study, we investigated the cytoprotective efficacy of morin, a natural flavonoid, against oxidative stress and elucidated the underlying mechanisms in C2C12 myoblasts. Our results indicated that morin treatment prior to hydrogen peroxide (H2O2) exposure significantly increased cell viability and prevented the generation of reactive oxygen species. H2O2-induced comet-like DNA formation and gamma H2AX phosphorylation were also markedly suppressed by morin with a parallel inhibition of apoptosis in C2C12 myoblasts, suggesting that morin prevented H2O2-induced cellular DNA damage. Furthermore, morin markedly enhanced the expression of heme oxygenase-1 (HO-1) associated with the induction and phosphorylation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and the inhibition of Kelch-like ECH-associated protein 1 (Keapl) expression. Notably, these events were eliminated by transient transfection with Nrf2-specific small interfering RNA. Additional experiments demonstrated that the activation of the Nrf2/HO-1 pathway by morin was mediated by the extracellular signal-regulated kinase (ERK) signaling cascade. This phenomenon was confirmed with suppressed Nrf2 phosphorylation and consequently diminished HO-1 expression in cells treated with a pharmacological inhibitor of ERK. Collectively, these results demonstrated that morin augments the cellular antioxidant defense capacity through the activation of Nrf2/HO-1 signaling, which involves the activation of the ERK pathway, thereby protecting C2C12 myoblasts from H2O2,-induced oxidative cytotoxicity.</P>
Choi, Si‐,Hwan,Park, Sung Jun,Cha, Guang‐,Ho,Quan, Juan Hua,Chang, Nam‐,Sik,Ahn, Myoung‐,Hee,Shin, Dae‐,Whan,Lee, Young‐,Ha Blackwell Publishing Ltd 2011 Acta ophthalmologica Vol.89 No.4
<P><B>Abstract.</B></P><P><B>Purpose: </B> Toxoplasmosis, which is caused by the protozoan parasite <I>Toxoplasma gondii</I>, can lead to severe visual impairment. <I>T.?gondii</I> inhibits or delays programmed cell death caused by various apoptotic triggers; however, the mechanisms involved in the <I>T</I>.?<I>gondii</I>‐induced suppression of apoptosis in retinal cells have not been analysed in detail.</P><P><B>Methods: </B> We investigated the role of <I>T</I>.<I>?gondii</I> infection in H<SUB>2</SUB>O<SUB>2</SUB>‐induced apoptosis in human retinal pigment epithelial cells (ARPE‐19) by monitoring the activities of apoptosis‐regulating molecules and mitogen‐activated protein kinases (MAPKs), including p38 MAPK. We also examined the gene downstream from p38 MAPK.</P><P><B>Results: </B> <I>T.?gondii</I> infection significantly inhibited the cellular toxicity of H<SUB>2</SUB>O<SUB>2</SUB> (500 μ<SMALL>m</SMALL>) and increased cell viability in a multiplicity of infection (MOI)‐dependent manner by reducing DNA fragmentation and reactive oxygen species (ROS) generation in ARPE‐19 cells. Western blot analysis also showed that <I>T</I>.?<I>gondii</I> infection prevented the host cell expression of pro‐apoptotic factors, such as Bad and Bax, and the activation of caspase‐3. Infection with <I>T</I>.?<I>gondii</I> increased the expression of the anti‐apoptotic factor Bcl‐2 in ARPE‐19 cells under oxidative stress. In accordance with these findings, <I>Toxoplasma</I> infection was protective enough to suppress the phosphorylation of p38 MAPK following H<SUB>2</SUB>O<SUB>2</SUB> treatment. Exposure to H<SUB>2</SUB>O<SUB>2</SUB> increased the expression of heme oxygenase‐1 (HO‐1) in ARPE‐19 cells, and its expression was significantly inhibited in H<SUB>2</SUB>O<SUB>2</SUB>‐treated infected cells.</P><P><B>Conclusion: </B> The protective function of <I>T</I>.?<I>gondii</I> infection against ROS‐induced apoptosis results from changes in the expression of apoptotic molecules and the downregulation of stress‐induced intracellular signalling.</P>
Cha, Kwang-Ho,Lee, Na-Young,Kim, Min-Soo,Kim, Jeong-Soo,Park, Hee-Jun,Park, Jun-Sung,Cho, Won-Kyung,Hwang, Sung-Joo The Korean Society of Pharmaceutical Sciences and 2010 Journal of Pharmaceutical Investigation Vol.40 No.5
The objectives of this study were to evaluate the effect of formulation ingredients on the drug release and to optimize the novel sustained release matrix tablet formulations of bupropion hydrochloride. A three factor, three-level Box-Behnken design was used for the optimization procedure, with the amounts of PEO ($X_1$), citric acid ($X_2$) and Compritol 888 ATO ($X_3$) as the independent variables. The selected dependent variables were the cumulative percentage values of bupropion hydrochloride that had dissolved after 1, 4 and 8 hr. Various dissolution profiles of the drug from sustained release matrix tablets were obtained. Optimization was performed for $X_1$, $X_2$ and $X_3$ using the following target ranges; $30%{\leq}Y_1{\leq}45%$; $70{\leq}Y_2{\leq}85%$; $85%{\leq}Y_3{\leq}100%$. The optimized formulation for bupropion hydrochloride was achieved with 12.5% PEO ($X_1$), 2.5% citric acid ($X_2$) and 10% Compritol 888 ATO ($X_3$). The sustained release matrix tablets with the optimized formulation provided a release profile that was close to predicted values. In addition, the dissolution profiles of the sustained release matrix tablet with the optimized formulation were similar to those of the commercial product Wellbutrin$^{(R)}$ SR tablets ($f_2$=79.83).