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Kim, Byung Hak,Roh, Eunmiri,Lee, Hwa Young,Lee, In-Jeong,Ahn, Byeongwoo,Jung, Sang-Hun,Lee, Heesoon,Han, Sang-Bae,Kim, Youngsoo American Society for Pharmacology and Experimental 2008 Molecular pharmacology Vol.73 No.4
<P>Benzoxathiole derivatives have been used in the treatment of acne and have shown cytostatic, antipsoriatic, and antibacterial properties. However, little is known about the molecular basis for these pharmacological properties, although nuclear factor (NF)-kappaB activation is closely linked to inflammation and cell proliferation. Here, we demonstrate that the novel small-molecule benzoxathiole 6,6-dimethyl-2-(phenylimino)-6,7-dihydro-5H-benzo-[1,3]oxathiol-4-one (BOT-64) inhibits NF-kappaB activation with an IC(50) value of 1 muM by blocking inhibitory kappaB(IkappaB) kinase beta (IKKbeta), and suppresses NF-kappaB-regulated expression of inflammatory genes in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. BOT-64 inhibits IKKbeta-mediated IkappaBalpha phosphorylation in LPS-activated macrophages, resulting in sequential prevention of downstream events, including proteolytic degradation of IkappaBalpha, DNA binding ability, and transcriptional activity of NF-kappaB. BOT-64 inhibits LPS-inducible IKKbeta activity in the cells and catalytic activity of highly purified IKKbeta. Moreover, the effect of BOT-64 on cell-free IKKbeta was abolished by substitution of Ser-177 and Ser-181 residues in the activation loop of IKKbeta to glutamic acid residues, indicating a direct interaction site of benzoxathiole. BOT-64 attenuates NF-kappaB-regulated expression of inflammatory genes such as inducible nitric-oxide synthase, cyclooxygenase-2, tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-6 in LPS-activated or expression vector IKKbeta-transfected macrophages. Furthermore, BOT-64 dose-dependently increases the survival rates of endotoxin LPS-shocked mice.</P>
Kim, Byung-Wook,More, Sandeep Vasant,Yun, Yo-Sep,Ko, Hyun-Myung,Kwak, Jae-Hwan,Lee, Heesoon,Suk, Kyoungho,Kim, In-Su,Choi, Dong-Kug Springer Science and Business Media LLC 2016 Acta pharmacologica Sinica. Vol.37 No.3
<P>Aim: To investigate the anti-neuroinflammatory activity of a novel synthetic compound, 7-methylchroman-2-carboxylic acid N-(2-trifluoromethyl) phenylamide (MCAP) against LPS-induced microglial activation in vitro. Methods: Primary mouse microglia and BV2 microglia cells were exposed to LPS (50 or 100 ng/mL). The expression of iNOS and COX-2, proinflammatory cytokines, NF-kappa B and p38 MAPK signaling molecules were analyzed by RT-PCR, Western blot and ELISA. The morphological changes of microglia and nuclear translocation of NF-kappa B were visualized using phase contrast and fluorescence microscopy, respectively. Results: Pretreatment with MCAP (0.1, 1, 10 mu mol/L) dose-dependently inhibited LPS-induced expression of iNOS and COX-2 in BV2 microglia cells. Similar results were obtained in primary microglia pretreated with MCAP (0.1, 0.5 mu mol/L). MCAP dose-dependently abated LPS-induced release of TNF-alpha, IL-6 and IL-1 beta, and mitigated LPS-induced activation of NF-kappa B by reducing the phosphorylation of I kappa B alpha in BV2 microglia cells. Moreover, MCAP attenuated LPS-induced phosphorylation of p38 MAPK, whereas SB203580, a p38 MAPK inhibitor, significantly potentiated MCAP-caused inhibition on the expression of MEF-2 (a transcription factor downstream of p38 MAPK). Conclusion: MCAP exerts anti-inflammatory effects in murine microglia in vitro by inhibiting the p38 MAPK and NF-kappa B signaling pathways and proinflammatory responses. MCAP may be developed as a novel agent for treating diseases involving activated microglial cells.</P>
김희순 ( Heesoon Kim ) 한국도시지리학회 2016 한국도시지리학회지 Vol.19 No.3
본고에서는 아바나의 형성 및 발달 과정을 스페인 식민제국의 조직과 운영 과정과 관련하여 연구하였다. 식민시기 아바나의 성장에는 스페인 왕실의 중앙집권적 통치체제 확립이 가장 중요한 동력으로 작용하였다. 이는 여타 스페인 제국의 도시와는 구분되는 독특한 성장 원인으로 아바나의 도시 구조, 도시 경제, 도시 사회 등에 영향을 미쳤다. 스페인 왕실은 정복한 식민지에 대한 왕실의 권력을 강화하고 지배 구조를 중앙집권화하고자 부왕령을 설치하였으며 부왕령들과 스페인의 중간 기지로서 쿠바와 아바나를 이용하였다. 또한 스페인 왕실은 플로타 제도를 통해 스페인과 식민지를 오가는 무역 노선을 왕실의 통제하에 둠으로써 식민지 경제의 중앙집권화를 꾀하였다. 해적의 피해를 막기 위해 시작된 플로타 시스템은 해적들이 아바나를 공격하게 하는 원인을 제공하였으며 이에 아바나는 방어시설이 시가지 성장의 중심 축이 되는 도시로 성장하였다. 1762~1763년 영국의 아바나 점령 이후 스페인 왕실은 부르봉 개혁을 통해 식민지에 대한 통제력을 높이고 새로운 부를 창출하고자 하였으며 이는 아바나의 경제 및 공간적 성장의 원인이 되었다. 18세기 말 아이티 혁명의 영향으로 쿠바의 설탕 산업이 발달하였으며 아바나는 설탕 생산의 중심지가 되었다. 이렇듯 아바나의 도시 성장 동력은 도시 내부나 배후지에서 형성된 것이 아니라 식민지배 및 권력의 중앙집권화라는 외부에서 도래한 체제적인 측면의 것이었고, 이로 인해 아바나는 도시의 형성부터 성장, 경제적 발전 등에서 스페인 식민제국의 여타 도시와는 다른 특성을 지닌 도시로 발달하였다. This paper studied the formation and development of Havana as an operation tool for Spanish Imperial. During the colonial period, the establishment of centralized authoritarian system of Spanish monarch has been Havana`s development motivity. This motivity influenced Havana`s urban system, economy, and society and it made difference between Havana and other Spanish colonial cities. Spanish monarch had established the viceroyalty system as means of reinforcement of royal power and consolidation of centralized ruling structure in the Spanish Imperial and appointed Havana as a hub spot. Spanish monarch had managed her centralized colonial economy by the regulation of trade through the flota system. As a center point of flota system, Havana had been attacked by the Caribbean pirates and it made Havana a fortified city. English occupation of Havana during 1762~1763 provided a momentum of Spanish monarch`s Bourbon reform. By Bourbon reform, Spanish monarch intended to tighten the control of America colony and advance new source of wealth in America, and it propelled Havana`s economic and urban development. In the end of the 18th century, Havana got an impetus of the development of the sugar industry by the Haitian Revolution. The origin of urban development of Havana stems from the outside of the city. Thus, it was the centralized colonial system of Spanish Imperial and it made Havana a noticeable city.
Hak Kim, Byung,Lee, Kum-Ho,Chung, Eun Yong,Chang, Yoon Sook,Lee, Heesoon,Lee, Chong-Kil,Min, Kyung Rak,Kim, Youngsoo Elsevier 2006 european journal of pharmacology Vol.543 No.1
<P><B>Abstract</B></P><P>6-Hydroxy-7-methoxychroman-2-carboxylic acid (3-nitrophenyl)amide (CP-1158) is a synthetic chroman carboxamide with trolox-like chemical structure. In the present study, CP-1158 was found to inhibit interleukin (IL)-6 production in lipopolysaccharide (LPS)-stimulated macrophages RAW 264.7. The CP-1158 attenuated LPS-induced synthesis of IL-6 transcript but also inhibited LPS-induced IL-6 promoter activity. Further, CP-1158 attenuated LPS-induced syntheses of tumor necrosis factor (TNF)-α, IL-1β, interferon-inducible protein (IP)-10 and macrophage inflammatory protein (MIP)-1β transcripts. Nuclear factor (NF)-κB has been evidenced to play a major mechanism in LPS-induced expression of IL-6 or other inflammatory cytokines. CP-1158 prevented LPS-induced nuclear translocation of NF-κB complex and subsequently inhibited DNA binding activity of NF-κB complex as well as NF-κB transcriptional activity in macrophages RAW 264.7. However, CP-1158 did not affect LPS-induced phosphorylation and degradation of inhibitory κB (IκB). In another experiment, CP-1158 inhibited IL-6 promoter activity elicited by expression vectors encoding NF-κB p50 or p65 subunit. Taken together, CP-1158 inhibited LPS-induced expression of inflammatory cytokines including IL-6, targeting NF-κB activating pathway downstream IκB degradation, and thus could provide an anti-inflammatory potential of chroman carboxamide.</P>
메틸크로만-2-카르복실산 N-(이치환)페닐아마이드 유도체의 NF-κB 저해 구조-활성 상관 관계
김태정(Tae-Jeong Kim),곽재환(Jae-Hwan Kwak),김영수(Youngsoo Kim),정재경(Jae-Kyung Jung),이희순(Heesoon Lee) 대한약학회 2011 약학회지 Vol.55 No.2
During the search for a novel compound that can inhibit NF-κB activation, 6-hydroxy-7-methoxychroman-2- carboxylic acid phenyl amide (KL-1156) was identified as a good inhibitor of NF-κB activation. In the present study, we describe the synthesis of methylchroman-2-carboxylic acid N-(disubstituted)phenylamide derivatives (1 and 2 serieses). In addition, their inhibitory effects of NF-κB are compared with activity of KL-1156 and SAR (structure activity relationship) are explored.