도토리 추출물의 3T3-L1 세포 분화억제 효과

김지연,이진,이창원,김애정,Kim, Ji-Yeon,Lee, Jin,Lee, Chang-Won,Kim, Ae-Jung 한국식품영양학회 2015 韓國食品營養學會誌 Vol.28 No.4

본 연구에서는 만성질환의 주요 위험인자인 비만을 예방하기 위한 식품소재로서 3T3-L1세포를 이용하여 탈피한 도토리의 항비만 효과를 알아보고자 하였다. 3T3-L1 세포에서 생존율(MTT assay)을 측정한 결과, AE와 AW 시료 모두 $500{\mu}g/mL$ 농도에서는 다소 생존율의 감소를 보여, $300{\mu}g/mL$를 최종 농도로 정하였다. 3T3-L1 세포의 지질축적 억제 효과를 측정한 결과, 농도 $100{\mu}g/mL$로 처리하였을 때 두 시료 모두 지질축적량의 증가를 보였으나, $200{\mu}g/mL$ 처리농도에서 AE 시료는 82%로, AW 시료는 74%로 감소되다가 $300 {\mu}g/mL$ 농도에서는 두 시료 모두 약 53% 수준까지 지질축적이 억제되었다. 3T3-L1 세포에서 중성지방 억제 효과를 확인한 결과, AE 시료의 경우 $200{\mu}g/mL$ 농도에서 11%의 감소율, $300{\mu}g/mL$ 농도에서 42% 수준의 감소율을 보였다. AW 시료도 $200{\mu}g/mL$ 농도에서 5%의 감소율과 $300{\mu}g/mL$에서 41%의 감소율을 보였다. 3T3-L1 세포의 ROS 생성량을 측정한 결과, 시료 농도 $200{\mu}g/mL$에서 AE는 42%, AW는 33%로 $300{\mu}g/mL$에서는 AE는 58%, AW는 52%로 ROS 생성량의 억제를 보였다. 3T3-L1 세포에서 mRNA 발현에 미치는 영향을 대조군과 비교하였을 때 두 시료(AE와 AW) 모두 $300{\mu}g/mL$ 농도에서 $PPAR-{\gamma}$은 54%와 38%, aP2는 40%와 18% 수준의 발현을 억제시키는 것으로 나타났다. 이상의 결과로 볼 때 탈피한 도토리는 3T3-L1 세포의 분화를 억제함으로써 새로운 항비만 소재로의 가능성이 있는 것으로 판단된다. This study aimed to investigate the suppressive effect of acorn extracts, by evaluating 70% ethanol extract (AE) and hot water extract (AW) using 3T3-L1 preadipocytes. We applied various levels (0, 100, 200, 300 and $500 {\mu}g/mL$) of AE and AW to 3T3-L1 preadipocytes. The cell viability of the 3T3-L1 preadipocytes was not affected by up $300 {\mu}g/mL$ of extracts, but was suppressed by level $500{\mu}g/mL$ of both AE and AW by 20% and 9% respectively. The accumulation of lipid droplets in differentiated 3T3-L1 preadipocytes was dose-dependently suppressed by AE and AW. Especially, at high concentrations ($300{\mu}g/mL$), AE (42%) was more effective than AW (41%). Reactive oxygen species (ROS) was also dose-dependently suppressed by treatment with AE (58%) and AW (52%). With regard to the mRNA related to differentiated 3T3-L1 preadipocytes, $PPAR-{\gamma}$ and aP2 were suppressed by treatment with AE (54 and 40%) and AW (38 and 18%). From our results, acorn extract (AE) has more suppressive effects than AW in differentiated 3T3-L1 preadipocytes. We therefore concluded that acorn has suppressive effects against obesity in differentiated 3T3-L1 cells due to antioxidation.

Aspergillus 속 미생물에 의한 발효비지의 항비만 효과

이상일(Lee, Sang-Il),이예경(Lee, Ye-Kyung),김순동(Kim, Soon-Dong),임종환(Lim, Jong-Hwan),서주원(Seo, Ju-Won),이인애(Lee, In-Ae) 한국산학기술학회 2013 한국산학기술학회논문지 Vol.14 No.11

고지방식이로 비만을 유도한 ICR 생쥐를 동물 모델로 하여 7종의 Aspergillus속 미생물로 발효시킨 발효비지 의 항비만 효과를 조사하였다. 수컷 ICR 생쥐에 5주간 고지방 식이를 실시하여 비만을 유도하고 고지방식이에 발효 비지 2%를 첨가하여 6주 동안 사육하였으며, 체중, 섭취량, 혈청 총콜레스테롤, 중성지질, Alanine transaminase과 high-density lipoprotein cholesterol, 간성 glutathione과 lipid peroxide를 측정하였다. 체중의 경우에 AE4 발효 비지를 식이한 군에서 가장 많이 감소 (31.33%, P<0.05)하였고 간성 GSH와 ALT증가로 고지방혈증이 저해되었다. 이상의 결 과로부터 Aspergillus속 미생물로 발효시킨 발효비지는 항비만 효과가 있는 것으로 나타났으며, 나아가 인체에서도 유 의한 비만개선 작용을 기대할 수 있을 것으로 사료된다. The anti-obesity effect of soybean curd residues (biji) fermented by seven Aspergillus spp. was investigated with obese ICR mice fed a high-fat diet. After inducing obesity by feeding high-fat diet for 5 weeks, animals were fed with a high fat diet supplemented with 2% fermented soybean curd residues for 6 weeks. Total cholesterol, triglyceride, Alanine transaminase, high-density lipoprotein cholesterol, hepatic content of glutathione and lipid peroxide were determined. In the case of body weight, AE4 group showed most prominent decrease (31.33%, P<0.05) and increase of hepatic GSH and ALT demonstrated hyperlipidemia inhibition. From the results, it is concluded that soybean curd residues fermented by Aspergillus spp. has anti-obesity effect and it is thought that fermented soybean curd resides can reduce obesity in human significantly.

상수원수 수질변화에 따른 전오존 처리효과 및 경제성 평가

최동훈 ( Dong Hoon Choi ),박진식 ( Jin Sik Park ),문추연 ( Choo Yeun Moon ),이재용 ( Jae Yong Lee ),유동춘 ( Dong Choon Ryu ),장성호 ( Seong Ho Jang ),권기원 ( Ki Won Kwon ),이수애 ( Soo Ae Lee ) 한국환경과학회 2013 한국환경과학회지 Vol.22 No.4

This study, changes in raw water quality is to indicate on the efficiency of ozone treatment of each pollutant as compared to derive the appropriate operating measures. The appropriate selection for injection rate of pre-ozone and did not inject pre-ozone assess changes in the water. When good water quality, you not injected of pre-ozone to evaluate the economic efficiency of electricity and put the most cost-effective ozone concentration were evaluated. Evaluation remove organic matter and chlorophyll-a concentration level in experiments with each factor of the water DOC> 2.5㎎ / L, THMFP> 70㎍ / L, Chl-a> 30㎎/㎥or less constant process, if you do not need to put pre-ozone showed little impact. It also does not put you in pre-ozone appropriate produce enough power rate savings was calculated as approximately 90 million won. Ability to remove organic materials and the ability to produce disinfection byproducts, and cost-effective decisions by considering the concentration of injection if pre-ozone 1 mg/L was investigated by the appropriate concentration of ozone injection.

Characteristics of bed-log of shiitake damaged by Bjerkandera adusta and antagonism between these two fungi

Won-Chull Bak,Bong-Hun Lee,Young-Ae Park,Hyun-Seok Kim 한국버섯학회 2010 한국버섯학회 국제학술대회 Vol.6 No.-

Simultaneous dual-frequency radio observations of S5 0716+714: A search for intraday variability with the Korean VLBI Network

Lee, Jee Won,Sohn, Bong Won,Byun, Do-Young,Lee, Jeong Ae,Kim, Sungsoo S. EDP Sciences 2017 Astronomy and astrophysics Vol.601 No.-

Academic Session Session 5 Hotel and Tourism Marketing I

Won-ae Cho,Young-Suk An,Suk-Bin Cha,Soon-Hee Kim,Hyung-Ryong Lee,Wanmin Kim,Sangwook Bae,Soyoung Park,Bo-Mi Lee,Ki-Joon Kwon,Hyung-Ryong Lee,Wonae Cho 한국마케팅과학회 2008 한국마케팅과학회 학술대회 발표 논문집 Vol.- No.-

Janex-1, a JAK3 inhibitor, ameliorates tumor necrosis factor-α-induced expression of cell adhesion molecules and improves myocardial vascular permeability in endotoxemic mice.

Lee, Jung Eun,Lee, Ae Sin,Kim, Duk Hoon,Jung, Yu Jin,Lee, Sik,Park, Byung-Hyun,Lee, Sun Hwa,Park, Sung Kwang,Kim, Won,Kang, Kyung Pyo D.A. Spandidos 2012 International journal of molecular medicine Vol.29 No.5

<P>Vascular endothelial cells play an important role in leukocyte trafficking during the inflammatory process. Proinflammatory cytokines activate the expression of cell adhesion molecules in endothelial cells. Janus kinase (JAK) and signal transducer and activator of transcription (STAT) are important intracellular cytokine signaling molecules that are involved in immune responses. The purpose of this study was to investigate the effect of JAK3 inhibition on the expression of tumor necrosis factor (TNF)-α-induced cell adhesion molecules in vascular endothelial cells and to evaluate the therapeutic potential of JAK3 for myocardial vascular permeability in endotoxemic mice. A JAK3 inhibitor, JANEX-1, decreased the TNF-α-induced expression of intercellular adhesion molecule (ICAM)-1, VCAM (vascular cell adhesion molecule)-1 and fractalkine in human umbilical vein endothelial cells (HUVECs). The downregulation of the expression of these cell adhesion molecules by JANEX-1 was mediated via suppression of STAT3 phosphorylation and nuclear factor-κB (NF-κB) activation. In endotoxemic mice, pretreatment with JANEX-1 prevented not only an increase in the cardiac ICAM-1 expression by LPS in the arteriolar and capillary endothelial cells, but also myocardial vascular leakage. These results suggest that inhibition of the JAK/STAT pathway by JANEX-1 ameliorates the expression of TNF-α-induced cell adhesion molecules in HUVECs and improves myocardial vascular permeability.</P>

COMP-angiopoietin-1 ameliorates inflammation-induced lymphangiogenesis in dextran sulfate sodium (DSS)-induced colitis model

Lee, Ae Sin,Sung, Mi Jeong,Kim, Won,Jung, Yu Jin Springer Berlin Heidelberg 2018 Journal of molecular medicine Vol.96 No.5

<P><B>Abstract</B></P><P>Alterations in the intestinal lymphatic network are pathological processes as related to inflammatory bowel disease (IBD). In this study, we demonstrated that reduction in inflammation-induced lymphangiogenesis ameliorates experimental acute colitis. A soluble and stable angiopoietin-1 (Ang1) variant, COMP-Ang1, possesses anti-inflammatory and angiogenic effects. We investigated the effects of COMP-Ang1 on an experimental colonic inflammation model. Experimental colitis was induced in mice by administering 3% dextran sulfate sodium (DSS) via drinking water. We determined body weight, disease activity indices, histopathological scores, lymphatic density, anti-ER-HR3 staining, and the expression of members of the vascular endothelial growth factor (VEGF) family and various inflammatory cytokines in the mice. The density of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) and VEGFR-3-positive lymphatic vessels increased in mice with DSS-induced colitis. We observed that COMP-Ang1-treated mice showed less weight loss, fewer clinical signs of colitis, and longer colons than Ade-DSS-treated mice. COMP-Ang1 also significantly reduced the density of LYVE-1-positive lymphatic vessels and the disruption of colonic architecture that is normally associated with colitis and repressed the immunoregulatory response. Further, COMP-Ang1 treatment reduced both M1 and M2 macrophage infiltration into the inflamed colon, which involved inhibition of VEGF-C and D expression. Thus, COMP-Ang1, which acts by reducing inflammation-induced lymphangiogenesis, may be used as a novel therapeutic for the treatment of IBD and other inflammatory diseases.</P><P><B>Key messages</B></P><P><P>COMP-Ang1 decreases inflammatory-induced lymphangiogenesis in experimental acute colitis.</P><P>COMP-Ang1 improves the symptom of DSS-induced inflammatory response.</P><P>COMP-Ang1 reduces the expression of pro-inflammatory cytokines in inflamed colon.</P><P>COMP-Ang1 reduces the expression of VEGFs in inflamed colon.</P><P>COMP-Ang1 prevents infiltration of macrophages in a DSS-induced colitis model.</P></P><P><B>Electronic supplementary material</B></P><P>The online version of this article (10.1007/s00109-018-1633-x) contains supplementary material, which is available to authorized users.</P>

Paricalcitol attenuates lipopolysaccharide-induced myocardial inflammation by regulating the NF-κB signaling pathway

LEE, AE SIN,JUNG, YU JIN,THANH, TÙ,NG NGUYỄ,N,LEE, SIK,KIM, WON,KANG, KYUNG PYO,PARK, SUNG KWANG UNKNOWN 2016 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.37 No.4

<P>Vitamin D deficiency is associated with an increased risk of cardiovascular disease, diabetes, colon and breast cancer, infectious diseases and allergies. Vascular alterations are an important pathophysiological mechanism of sepsis. Experimental data suggest that paricalcitol, a vitamin D2 analogue, exerts beneficial effects on renal inflammation and fibrosis. In the present study, we aimed to investigate the effects of paricalcitol on lipopolysaccharide (LPS)-induced myocardial inflammation and to elucidate the underlying mechanisms. We used primary cultured human umbilical vein endothelial cells for <I>in vitro</I> experiments, in which stimulation with tumor necrosis factor (TNF)-α was used to induce endothelial cell inflammation. For <I>in vivo</I> experiments, myocardial inflammation was induced by an intraperitoneal injection of 15 mg/kg LPS into C57BL6 mice pre-treated with or without 0.2 <I>µ</I>g/kg paricalcitol. Treatment with paricalcitol suppressed the TNF-α-induced increase in the protein expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and fractalkine in endothelial cells. Treatment with paricalcitol also decreased the TNF-α-induced nuclear factor (NF)-κB binding activity. In a mouse model of LPS-induced myocardial inflammation, pre-treatment with paricalcitol prevented the LPS-induced increase in the expression of myocardial ICAM-1, phosphorylated p65 and myocardial TNF-α. Pre-treatment with paricalcitol also alleviated endotoxemia-induced microvascular leakage in the myocardium. The findings of our study suggest that paricalcitol exerts a protective effect against LPS-induced myocardial inflammation by regulating the expression of cell adhesion molecules and TNF-α, and by improving myocardial permeability.</P>

Activation of the Nrf2 signaling pathway and neuroprotection of nigral dopaminergic neurons by a novel synthetic compound KMS99220

Lee, Ji Ae,Son, Hyo Jin,Choi, Ji Won,Kim, Jinwoo,Han, Se Hee,Shin, Nari,Kim, Ji Hyun,Kim, Soo Jeong,Heo, Jun Young,Kim, Dong Jin,Park, Ki Duk,Hwang, Onyou Elsevier 2018 Neurochemistry International Vol.112 No.-

<P><B>Abstract</B></P> <P>The transcription factor Nrf2 is known to induce gene expression of antioxidant enzymes and proteasome subunits. Because both oxidative stress and protein aggregation have damaging effects on neurons, activation of the Nrf2 signaling should be beneficial against neurodegeneration. In this study, we report a novel synthetic morpholine-containing chalcone KMS99220 that confers neuroprotection. It showed high binding affinity to the Nrf2 inhibitory protein Keap-1 and increased nuclear translocation of Nrf2 and gene expression of the antioxidant enzymes heme oxygenase-1, NAD(P)H:quinone oxidoreductase-1, and the catalytic and modifier subunits of glutamate-cysteine ligase in dopaminergic CATH.a cells. KMS99220 also increased expression of the proteasome subunits PSMB5, PSMB7, PSMB8 and PSMA1, and the respective chymotrypsin and trypsin-like proteasomal enzyme activities, and reduced α-synuclein aggregate in GFP-α-syn A53T-overexpressing cells. KMS99220 exhibited a favorable pharmacokinetic profile with excellent bioavailability and metabolic stability, did not interfere with activities of the cytochrome p450 isotypes, and showed no apparent in vivo toxicity when administered up to 2000 mg/kg. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice, oral administration of KMS99220 prevented degeneration of the nigral dopaminergic neurons, induced the Nrf2 target genes, and effectively prevented the associated motor deficits. These results suggest KMS99220 as a potential candidate for therapy against Parkinson's disease.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We synthesized a novel compound KMS99220 that activates the Nrf2 signaling pathway. </LI> <LI> KMS99220 elevates Nrf2-dependent gene expression of HO-1, NQO1 and GCLM/GCLC. </LI> <LI> It raises expression and activities of proteases and lowers α-synuclein aggregation. </LI> <LI> It prevents nigral dopaminergic neurodegeneration and motor deficits in MPTP mice. </LI> <LI> It exhibits favorable pharmacokinetics, bioavailability and metabolic stability. </LI> </UL> </P>