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( Young Il Kim ),( Seung Won Park ),( Jeong Hwee Choi ),( Myong Il Bae ),( Min Kyung Shin ),( Mu Hyoung Lee ) 대한피부과학회 2013 대한피부과학회 학술발표대회집 Vol.65 No.2
Background: Activins are dimeric growth and differentiation factors which belong to the transforming growth factor-β (TGF-β) superfamily. Objectives: To know the mechanism how activin regulates transcription of lipopolysaccharide (LPS)-induced Toll-like receptors (TLRs), cytokines, and inducible nitric oxide synthase (iNOS) in human melanocytes, and the involvement of nuclear transcription factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. Methods: Normal human melanocytes were pretreated with activin A before exposure to LPS. Total RNAs were purified and real-time PCR was performed. Also we conducted immunoblot analysis to know the expression levels of proteins. Results: LPS increased mRNA expressions of TLRs (1-10) and cytokines (IL-1β, IL-6, IL-8, IL-10, TNF-α), and enhanced mRNA and protein expression of iNOS. Activin inhibited LPS-induced mRNA expressions of TLRs and cytokines, and decreased mRNA and protein expression of LPS-induced iNOS. Also activin suppressed NF-κB p65 activation and blocked IκBα degradation in LPS-stimulated melanocytes, and reduced LPS-induced p38 MAPK and MEK/ERK activations. Conclusion: Activin inhibited expression of genes of TLRs, cytokines, and iNOS in LPS-activated normal human melanocytes. Moreover, anti-inflammatory effect of activin was mediated through suppressing activation of NF-κB and MAPKs signaling pathways in LPS-activated normal human melanocytes, resulting in reduced expression of TLRs, cytokines, and nitric oxide.
관절1호방이 Collagen Ⅱ로 유발된 관절염 억제에 관한 연구
한규진 ( Kyu Jin Han ),진광선 ( Kwang Seon Jin ),신혜란 ( Hye Ran Shin ),윤일지 ( Il Ji Yoon ),최승훈 ( Seung Hoon Choi ),오민석 ( Min Seok Oh ) 한방재활의학과학회 2005 한방재활의학과학회지 Vol.15 No.4
Objectives : The aim of this study was to know the immunity responses of Gwanjulbang-1(Quanjiefang-1)(hereinafter referred to GJB-1) to on Rheumatoid Arthritis in Collagen-induced Arthritis(CIA) Mice Methods : For this purpose, experiments were performed to measure the cytotoxicity against mLFC, hFLSs and the production of proinflammatory cytokines IL-1β, IL-6, TNF-α, IFN-γ in hFLSs and the production of pro-inflammatory cytokines IL-4, IL-10 and the value of CD3+(T), CD19+(B), CD3+/CD69+, CD4, γδ T cells, CD4+/CD25+ Results : 1. The cytotoxicity against mLFC, hFLSs were not measured. 2. The production of pro-inflammatory cytokines IFN-γ were reduced in hFLSs. 3. The production of pro-inflammatory cytokines IL-4, IL-10 were increased. 4. Statistically significant value of CD3+(T), CD19+(B), CD3+/CD69+, CD4, γδ T cells, CD4+/CD25+ compared with control group, wild type, MTX. Conclusions : Comparison of the results for this study showed that GJB-1 had immunomodulatory effects of suppressing or enhancing. So we expect that GJB-1 should be used as a effective drugs for not only rheumatoid arthritis but also another auto-immune disease. Therefore we have to survey continuously in looking for the effective substance and mechanism in the future.
CHOI, SUN-IL,JUNG, TAE-DONG,CHO, BONG-YEON,CHOI, SEUNG-HYUN,SIM, WAN-SUP,HAN, XIONGGAO,LEE, SANG JONG,KIM, YOUNG-CHEUL,LEE, OK-HWAN UNKNOWN 2019 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.44 No.2
<P> Processed products from agricultural produce generate a large number of agricultural by-products that contain a number of functional substances. These are often discarded owing to the lack of suitable processing methods. The present study investigated the anti-photoaging properties of fermented rice bran (FRB), soybean cake (FSB) and sesame seed cake (FSC) on ultraviolet B (UVB)-irradiated hairless mouse skin. Results indicated that the oral administration of FRB, FSB and FSC effectively inhibited the UVB irradiation-induced expression of matrix metalloproteinase (MMP)-2, MMP-9, MMP-3 and MMP-13. Reverse transcription-quantitative polymerase chain reaction results also demonstrated that FRB, FSB and FSC significantly inhibited the UVB-induced expression of the genes encoding tumor necrosis factor-α, inducible nitric oxide synthase, interleukin (IL)-6 and IL-1β when compared with the UVB-vehicle group (P<0.05). Additionally, collagen degradation and mast cell infiltration were reduced in hairless mouse skin. Furthermore, UVB-induced wrinkle formation was also significantly reduced in mouse skin compared with the UVB-vehicle group (P<0.05). These results reveal that fermented agricultural by-products may serve as potential functional materials with anti-photoaging activities. </P>
Choi, Seung‐,Hoon,Hwang, Daesub,Kim, Dong‐,Young,Kervella, Yann,Maldivi, Pascale,Jang, Sung‐,Yeon,Demadrille, Renaud,Kim, Il‐,Doo WILEY‐VCH Verlag 2013 Advanced Functional Materials Vol.23 No.25
<P>Highly porous amorphous Zn<SUB>2</SUB>SnO<SUB>4</SUB> electrodes are prepared using electrospinning techniques and combined with organic or ruthenium dyes to fabricate dye‐sensitized solar cells. As reported by Sung‐Yeon Jang, Renaud Demadrille, Il‐Doo Kim, and co‐workers on page 3146, the devices based on 3‐μm‐thick electrodes and the organic dyes demonstrate significantly improved performances compared to those using the ruthenium complex. Using this approach, solar cells with power conversion efficiencies up to 3.7% are obtained. </P>
Interleukin-2가 호산구 생존에 미치는 영향과 기전에 관한 연구
김효석 ( Hyo Seok Kim ),이영목 ( Young Mok Lee ),최영수 ( Young Soo Choi ),김경호 ( Kyung Ho Kim ),임건일 ( Geon Il Im ),문승혁 ( Jeong Sung Whan ),정성환 ( Moon Seung Hyug ),김현태 ( Hyeon Tae Kim ),어수택 ( Uh Soo Taek ),김용훈 대한결핵 및 호흡기학회 1996 Tuberculosis and Respiratory Diseases Vol.43 No.3
S-562 : MicroRNA-155 as a proinflammatory regulator in acute gouty arthritis
( Jung Ho Choi ),( Hye Mi Jin ),( Moon Ju Kim ),( Young Nan Cho ),( Kwang Il Nam ),( Seung Jung Kee ),( Jang Bae Moon ),( Dong Jin Park ),( Yong Wook Park ),( Shin Seok Lee ),( Tae Jong Ki ) 대한내과학회 2013 대한내과학회 추계학술대회 Vol.2013 No.1
Introduction: MicroRNA-155 (miR-155) is crucial for the proinflammatory activation of human myeloid cells and antigen-driven inflammatory arthritis. Since, the functional role of miR-155 in gouty arthritis has not been defined. The aim of this study was to examine the role of miR-155 in pathogenesis of gouty arthritis. Materials and methods: Samples from fourteen patients with gouty arthritis and ten healthy controls were obtained. Monosodium urate (MSU) crystals were prepared by recrystallization from uric acid. Total RNA was isolated using the miRNeasy kit (Qiagen). The miScript Reverse Transcription Kit (Qiagen) was used for cDNA preparation. MiScript primer assay (Qiagen) were used for semiquantitative determination of the expression of human miR-155. Human TNF-α and IL-1β in supernatants were measured by Luminex (Millipore, USA) according to the instructions of the manufacturer. Gout peritonitis mice (Male C57BL/6J) model used to analyze expressions of miR-155, Src homology 2-containing inositol phosphatase-1 (SHIP-1), and inflammatory cytokines. Results: The samples from gout patients proved to be highly enriched in miR-155, with levels of expression being 4-fold higher than those found in peripheral blood mononuclear cells (PBMC) from healthy controls and gout (p<0.05). miR-155 was found to be strongly induced by stimulation of MSU crystals after 24 hours and their expressions gradually decreased. Stimulating with MSU crystals for the indicated times, and the level of SHIP-1 was found to be gradually decreased in according to over-expression of miR-155. miR-155 promoted MSU-induced proinflammatory cytokine production. Commensurate with our observations in human synovial monocytes, miR-155 expression was elevated in gout mice model. SHIP-1 protein levels were markedly reduced in cells by MSU stimulated, compared to the control. MSU crystal induced peritonitis mice significantly increased the production of inflammatory cytokines, such as TNF-α and IL-1β. Conclusion: Overexpression of miR-155 in synovial fluid mononuclear cells (SFMC) led to down-regulation of SHIP-1 and an increase in the production of proinflammatory cytokines.
LPS로 유도한 RAW 264.7 세포의 염증반응에서 자초(紫草)의 항염증 효과
최선복 ( Sun Bok Choi ),배기상 ( Gi Sang Bae ),조일주 ( Il Joo Jo ),박경철 ( Kyoung Chel Park ),서승희 ( Seung Hee Seo ),김동구 ( Dong Goo Kim ),신준연 ( Joon Yeon Shin ),곽태신 ( Tae Sin Gwak ),이정현 ( Jung Hyun Lee ),이금산 ( G 대한본초학회 2013 大韓本草學會誌 Vol.28 No.2
Objective: Lithospermum Erythrorhizon (LE) has been used as an anti-bacterial and anti-inflammatory agent. However, it is unclear that LE aqueous extract could show the anti-inflammatory effects in RAW 264.7cells. The purpose of this study was to investigate the anti-inflammatory effect of aqueous extract from LE on lipopolysaccharide (LPS) - induced inflammatory response. Methods: To measure out the cytotoxicity of LE, we performed the MTT assay. To evaluate the anti-inflammatory effects of LE, we examined the inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokines (tumor necrosis factor (TNF)-a, interleukin, (IL)-1β and (IL)-6) on RAW 264.7 cells. We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor-B (NF-κB) activation by western blot. Results : Aqueous Extract from LE itself did not have any cytotoxic effect in RAW 264.7 cells. Aqueous extract from LE inhibited LPS-induced productions of inflammatory mediators such as NO, PGE2, and pro-inflammatory cytokines including TNF-a, IL-1β and IL-6 in RAW 264.7cells. In addition, LE inhibited the phosphorylation of p38 kinases (p38), c-Jun NH2-terminal kinase (JNK), and NF-κB activation in RAW 264.7 cells. Conclusion : LE down-regulated LPS-induced production of inflammatory mediators through the inhibition of p38, JNK and NF-κB activation. Taken together, these results could provide the evidence for the anti-inflammatory effects of LE. Therefore, LE may be a novel target in the management of inflammation and help to support a potential strategy for prevention and therapy of inflammatory diseases.
Kim, Seong-Ryeol,Song, Jae-Hyoung,Ahn, Jae-Hee,Lee, Geun-Shik,Ahn, Huijeong,Yoon, Sung-il,Kang, Seung Goo,Kim, Pyeung-Hyeun,Jeon, Sang-Min,Choi, Eun-Ji,Shin, Sooyoung,Cha, Younggil,Cho, Sungchan,Kim, Elsevier 2018 Antiviral research Vol.151 No.-
<P>Human rhinovirus (HRV) infection causes more than 80% of all common colds and is associated with severe complications in patients with asthma and chronic obstructive pulmonary disease. To identify antiviral drug against HRV infection, we screened 800 FDA-approved drugs and found budesonide as one of the possible drug candidates. Budesonide is a corticosteroid, which is commonly used to prevent exacerbation of asthma and symptoms of common cold. Budesonide specifically protects host cells from cytotoxicity following HRV infection, which depend on the expression of glucocorticoid receptor. Intranasal administration of budesonide lowered the pulmonary HRV load and the levels of IL-1 beta cytokine leading to decreased lung inflammation. Budesonide regulates IL-1 beta production following HRV infection independent of inflammasome activation. Instead, budesonide induces mitochondrial reactive oxygen species followed by activation of autophagy. Further, the inhibition of autophagy following chloroquine or bafilomycin Al treatment reduced the anti-viral effect of budesonide against HRV, suggesting that the antiviral activity of budesonide was mediated via autophagy. The results suggest that budesonide represents a promising antiviral and anti-inflammatory drug candidate for the treatment of human rhinovirus infection.</P>
Lee, Young-Sun,Yi, Hyon-Seung,Suh, Yang-Gun,Byun, Jin-Seok,Eun, Hyuk Soo,Kim, So Yeon,Seo, Wonhyo,Jeong, Jong-Min,Choi, Won-Mook,Kim, Myung-Ho,Kim, Ji Hoon,Park, Keun-Gyu,Jeong, Won-Il Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.11
Retinols are metabolized into retinoic acids by alcohol dehydrogenase (ADH) and retinaldehyde dehydrogenase (Raldh). However, their roles have yet to be clarified in hepatitis despite enriched retinols in hepatic stellate cells (HSCs). Therefore, we investigated the effects of retinols on Concanavalin A (Con A)-mediated hepatitis. Con A was injected into wild type (WT), Raldh1 knockout ($Raldh1^{-/-}$), $CCL2^{-/-}$ and $CCR2^{-/-}$ mice. For migration study of regulatory T cells (Tregs), we used in vivo and ex vivo adoptive transfer systems. Blockade of retinol metabolism in mice given 4-methylpyrazole, an inhibitor of ADH, and ablated Raldh1 gene manifested increased migration of Tregs, eventually protected against Con A-mediated hepatitis by decreasing interferon-${\gamma}$ in T cells. Moreover, interferon-${\gamma}$ treatment increased the expression of ADH3 and Raldh1, but it suppressed that of CCL2 and IL-6 in HSCs. However, the expression of CCL2 and IL-6 was inversely increased upon the pharmacologic or genetic ablation of ADH3 and Raldh1 in HSCs. Indeed, IL-6 treatment increased CCR2 expression of Tregs. In migration assay, ablated CCR2 in Tregs showed reduced migration to HSCs. In adoptive transfer of Tregs in vivo and ex vivo, Raldh1-deficient mice showed more increased migration of Tregs than WT mice. Furthermore, inhibited retinol metabolism increased survival rate (75%) compared with that of the controls (25%) in Con A-induced hepatitis. These results suggest that blockade of retinol metabolism protects against acute liver injury by increased Treg migration, and it may represent a novel therapeutic strategy to control T cell-mediated acute hepatitis.
Adiponectin is a negative regulator of NK cell cytotoxicity.
Kim, Kun-Yong,Kim, Jae Kwang,Han, Seung Hyun,Lim, Jong-Seok,Kim, Keun Il,Cho, Dae Ho,Lee, Myeong-Sok,Lee, Jeong-Hyung,Yoon, Do-Young,Yoon, Suk Ran,Chung, Jin Woong,Choi, Inpyo,Kim, Eunjoon,Yang, Young American Association of Immunologists 2006 Journal of Immunology Vol.176 No.10
<P>NK cells are a key component of innate immune systems, and their activity is regulated by cytokines and hormones. Adiponectin, which is secreted from white adipose tissues, plays important roles in various diseases, including hypertension, cardiovascular diseases, inflammatory disorders, and cancer. In this study the effect of adiponectin on NK cell activity was investigated. Adiponectin was found to suppress the IL-2-enhanced cytotoxic activity of NK cells without affecting basal NK cell cytotoxicity and to inhibit IL-2-induced NF-kappaB activation via activation of the AMP-activated protein kinase, indicating that it suppresses IL-2-enhanced NK cell cytotoxicity through the AMP-activated protein kinase-mediated inhibition of NF-kappaB activation. IFN-gamma enhances NK cell cytotoxicity by causing an increase in the levels of expression of TRAIL and Fas ligand. The production of IFN-gamma, one of the NF-kappaB target genes in NK cells, was also found to be suppressed by adiponectin, accompanied by the subsequent down-regulation of IFN-gamma-inducible TRAIL and Fas ligand expression. These results clearly demonstrate that adiponectin is a potent negative regulator of IL-2-induced NK cell activation and thus may act as an in vivo regulator of anti-inflammatory functions.</P>