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Ran Joo Choi,Eun Myoung Shin,Tran Minh Ngoc,Ki Hwan Bae,Yeong Shik Kim 한국당과학회 2011 한국당과학회 학술대회 Vol.2011 No.1
This study investigates the anti-inflammatory effects of several components isolated from Rheum tanguticum Maxim. (Polygonaceae). Previously, we found that 70 % ethanol extracts of Rheum Rhizoma (Rheum tanguticum, R. undulatum, R. palmatum, R. officinale, Rumex crispus) had anti-inflammatory properties on LPS-stimulated RAW 264.7 macrophages and carrageenan-induced paw edema model. Thus, we studied five anthraquinone derivatives isolated from Rheum tanguticum, including chrysophanol, chrysophanol-8-O-Glc, 2-methoxy-4-hydroxyanthraquinone-5-O-Glc, emodin, and physcion. Chrysophanol, chrysophanol-8-O-Glc, physcion and emodin inhibited nitric oxide (NO) production at micromolar concentrations in LPS-induced RAW 264.7 macrophages. Among these anthraquinones, emodin was found to be a potent inhibitor with its IC50 (the half maximal inhibitory concentration) value of 57.23 μM. In addition, these four compounds dose-dependently reduced inducible nitricoxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression conducted by Western blotting analysis. Taken together, our data suggest that chrysophanol, chrysophanol-8-O-Glc, physcion and emodin from R. tanguticum showed anti-inflammatory activities through their inhibition of iNOS and COX-2 expression. Emodin was already reported to exhibit anti-inflammatory effects especially on acute pacreatitis animal model (1-3). Therefore, the further study is required to clarify anti-inflammatory mechanism of emodin in detail.
Choi Min Joo,Choi Won Suk,Seong Hye,최준용,Kim Jong-Hyun,Kim Yae-Jean,Cho Eun Young,김동현,Park Hyesook,Lee Heeyoung,Kim Nam Joong,Song Joon Young,Cheong Hee Jin,Kim Sang Il,Peck Kyong Ran 대한의학회 2021 Journal of Korean medical science Vol.36 No.23
Background: This study presents a framework for determining the allocation and distribution of the limited amount of vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Methods: After analyzing the pandemic strategies of the major organizations and countries and with a literature review conducted by a core panel, a modified Delphi survey was administered to 13 experts in the fields of vaccination, infectious disease, and public health in the Republic of Korea. The following topics were discussed: 1) identifying the objectives of the vaccination strategy, 2) identifying allocation criteria, and 3) establishing a step-by-step vaccination framework and prioritization strategy based on the allocation criteria. Two rounds of surveys were conducted for each topic, with a structured questionnaire provided via e-mail in the first round. After analyzing the responses, a meeting with the experts was held to obtain consensus on how to prioritize the population groups. Results: The first objective of the vaccination strategy was maintenance of the integrity of the healthcare system and critical infrastructure, followed by reduction of morbidity and mortality and reduction of community transmission. In the initial phase, older adult residents in care homes, high-risk health and social care workers, and personal support workers who work in direct contact with coronavirus disease 2019 (COVID-19) patients would be prioritized. Expansion of vaccine supply would allow immunization of older adults not included in phase 1, followed by healthcare workers not previously included and individuals with comorbidities. Further widespread vaccine supply would ensure availability to the extended adult age groups (50–64 years old), critical workers outside the health sector, residents who cannot socially distance, and, eventually, the remaining populations. Conclusion: This survey provides the much needed insight into the decision-making process for vaccine allocation at the national level. However, flexibility in adapting to strategies will be essential, as new information is constantly emerging.
Protective role of DAX-1 deficiency against acetaminophen-induced liver injury in animal model
Young Joo Suh,Hyo Jeong Yun,Yu bin Kim,Eun Jung Kang,Dong Hee Choi,Jung Hyeon Choi,Young Keun Choi,In Bok Lee,Yun Jeong Seo,Jung Ran Noh,Yong Hoon Kim,Jong Soo Lee,Chul Ho Lee 한국실험동물학회 2022 한국실험동물학회 학술발표대회 논문집 Vol.2022 No.7
Rapid Dissemination of Newly Introduced Plasmodium vivax Genotypes in South Korea
Kim, Yeon-Joo,Kim, Jung-Yeon,Lee, Eun-Gyu,Lee, Byeong-Chul,Cho, Shin-Hyung,Yu, Jae-Ran,Rhie, Ho-Gun,Choi, Yien-Kyoung,Lee, Ho-Sa,Lee, Joo-Shil,Kim, Tong-Soo,Choi, Kyung-Mi,Park, Mi-Hyun American Society of Tropical Medicine and Hygiene 2010 The American journal of tropical medicine and hygi Vol.82 No.3
<P>Reemerged Plasmodium vivax malaria in South Korea has not yet been eradicated despite continuous governmental efforts. It has rather become an endemic disease. Our study aimed to determine the genetic diversity in P. vivax merozoite surface protein-1 (PvMSP-1) and circumsporozoite protein (PvCSP) genes over an extended period after its reemergence to its current status. Sequence analysis of PvMSP-1 gene sequences from the 632 P. vivax isolates during 1996-2007 indicates that most isolates recently obtained were different from isolates obtained in the initial reemergence period. There was initially only one subtype (recombinant) present but its subtypes have varied since 2000; six MSP-1 subtypes were recently found. A similar variation was observed by CSP gene analysis; a new CSP subtype was found. Understanding genetic variation patterns of the parasite may help to analyze trends and assess extent of endemic malaria in South Korea.</P>
Joo, Hee Kyoung,Lee, Yu Ran,Choi, Sunga,Park, Myoung Soo,Kang, Gun,Kim, Cuk-Seong,Jeon, Byeong Hwa The Korean Society of Pharmacology 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.4
Activation of protein kinase C (PKC) is closely linked with endothelial dysfunction. However, the effect of $PKC{\beta}II$ on endothelial dysfunction has not been characterized in cultured endothelial cells. Here, using adenoviral $PKC{\beta}II$ gene transfer and pharmacological inhibitors, the role of $PKC{\beta}II$ on endothelial dysfucntion was investigated in cultured endothelial cells. Phorbol 12-myristate 13-acetate (PMA) increased reactive oxygen species (ROS), p66shc phosphorylation, intracellular adhesion molecule-1, and monocyte adhesion, which were inhibited by $PKC{\beta}i$ (10 nM), a selective inhibitor of $PKC{\beta}II$. PMA increased the phosphorylation of CREB and manganese superoxide dismutase (MnSOD), which were also inhibited by $PKC{\beta}i$. Gene silencing of CREB inhibited PMA-induced MnSOD expression, suggesting that CREB plays a key role in MnSOD expression. Gene silencing of $PKC{\beta}II$ inhibited PMA-induced mitochondrial ROS, MnSOD, and ICAM-1 expression. In contrast, overexpression of $PKC{\beta}II$ using adenoviral $PKC{\beta}II$ increased mitochondrial ROS, MnSOD, ICAM-1, and p66shc phosphorylation in cultured endothelial cells. Finally, $PKC{\beta}II$-induced ICAM-1 expression was inhibited by Mito-TEMPO, a mitochondrial ROS scavenger, suggesting the involvement of mitochondrial ROS in PKC-induced vascular inflammation. Taken together, the results suggest that $PKC{\beta}II$ plays an important role in PMA-induced endothelial dysfunction, and that the inhibition of $PKC{\beta}II$-dependent p66shc signaling acts as a therapeutic target for vascular inflammatory diseases.
Choi, Joo Sun,Yoon, Taek Joon,Kang, Kyung Ran,Lee, Kyeong Ho,Kim, Won Ho,Suh, Young Ho,Song, Jihyun,Jung, Myeong Ho Pharmaceutical Society of Japan 2006 Biological & pharmaceutical bulletin Vol.29 No.2
<P>The protective effect of a 30 kDa glycoprotein (GF-AS) isolated from the stem bark of <I>Acanthopanax senticosus</I> against acute and chronic alcohol-induced hepatotoxicity were studied. N-terminal amino acid sequence of GF-AS showed NH<SUB>2</SUB>-Val-Ala-Tyr-Pro-Trp-Ala-Gly-Phe-Ala-Leu-Ser-Leu-Glx-Pro-Pro-Ala-Gly-Tyr-. GF-AS significantly increases the activities of alcohol-metabolizing enzymes, including alcohol dehydrogenase, microsomal ethanol metabolizing system, and acetaldehyde dehydrogenase in rats acutely treated with alcohol, resulting in decreased plasma alcohol levels. GF-AS also increases the activities of antioxidant enzymes and glutathione level. Markers of liver injury induced by alcohol: elevated serum levels of aspartate aminotransferase, alanine aminotransferase, triglyceride and cholesterol, are reduced by GF-AS in both acutely and chronically treated rats. The activities of lipogenic enzymes including malic enzyme, glucose-6-phosphate dehydrogenase, and 6-phosphoglucuronic acid dehydrogenase in chronic alcohol-treated rats are significantly decreased by GF-AS. Furthemore, GF-AS improves histological change in fatty liver and hepatic lesions induced by alcohol. Collectively, GF-AS may alleviate alcohol-induced hepatotoxicity through increasing ethanol and lipid metabolism, as well as antioxidant defense systems in livers injured by acute- and chronic-alcohol treatment.</P>
( Joo Ran Hong ),( Ji Youn Hong ),( Jin Hee Kim ),( Hye In Cheon ),( Min Seok Hur ),( Byung Gon Choi ),( Song Hee Han ),( Yang Won Lee ),( Yong Beom Choe ),( Kyu Joong Ahn ) 대한피부과학회 2018 대한피부과학회 학술발표대회집 Vol.70 No.2
Background: H1-antihistamines have been used widely to treat pruritus in atopic dermatitis (AD). Although the evidence for H1-antihistamine monotherapy for pruritus in AD is inconclusive, combination therapy with topical glucocorticoids are particularly considered as to be effective as both short-term intensive therapy and maintenance treatment in patients with frequent relapse. Objectives: We conducted a meta-analysis for confirming the efficacy of antihistamine as an adjunct to topical corticosteroid application in the treatment of AD. Methods: We identified 1,206 studies through systematically searching Medline, Embase, and CENTRAL databases for articles published from 1967 to 2015. Random effects meta-analysis was used to calculate mean differences (MD) with 95% confidence intervals (CI). Results: Two studies satisfying the inclusion criteria of antihistamine therapy with mandatory topical steroid use were selected. Comparing antihistamine monotherapy with combination therapy, patients treated with the addition of antihistamine to topical corticosteroids showed a statistically significant clinical improvement (standard MD, -0.24; 95% CI, -0.42 to -0.05; p = 0.01). Conclusion: This meta-analysis based on two studies suggests that antihistamine therapy as an adjunctive therapy for pruritus in AD may have beneficial effects in combination with topical corticosteroid treatment.
Joo, Hee Kyoung,Lee, Yu Ran,Kang, Gun,Choi, Sunga,Kim, Cuk-Seong,Ryoo, Sungwoo,Park, Jin Bong,Jeon, Byeong Hwa Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.12
Translocator protein 18 kDa (TSPO) is a mitochondrial outer membrane protein and is abundantly expressed in a variety of organ and tissues. To date, the functional role of TSPO on vascular endothelial cell activation has yet to be fully elucidated. In the present study, the phorbol 12-myristate 13-acetate (PMA, 250 nM), an activator of protein kinase C (PKC), was used to induce vascular endothelial activation. Adenoviral TSPO overexpression (10-100 MOI) inhibited PMA-induced vascular cell adhesion molecule-1 (VCAM-1) and intracellular cell adhesion molecule-1 (ICAM-1) expression in a dose dependent manner. PMA-induced VCAM-1 expressions were inhibited by Mito-TEMPO ($0.1-0.5{\mu}m$), a specific mitochondrial antioxidants, and cyclosporin A ($1-5{\mu}m$), a mitochondrial permeability transition pore inhibitor, implying on an important role of mitochondrial reactive oxygen species (ROS) on the endothelial activation. Moreover, adenoviral TSPO overexpression inhibited mitochondrial ROS production and manganese superoxide dismutase expression. On contrasts, gene silencing of TSPO with siRNA increased PMA-induced VCAM-1 expression and mitochondrial ROS production. Midazolam ($1-50{\mu}m$), TSPO ligands, inhibited PMA-induced VCAM-1 and mitochondrial ROS production in endothelial cells. These results suggest that mitochondrial TSPO can inhibit PMA-induced endothelial inflammation via suppression of VCAM-1 and mitochondrial ROS production in endothelial cells.