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Yang, Gabsik,Lee, Kyungjin,An, Duck-Gun,Lee, Mi-Hwa,Ham, In-Hye,Choi, Ho-Young Informa Healthcare 2012 Immunopharmacology and immunotoxicology Vol.34 No.3
<P>The flower of <I>Chrysanthemum boreale</I> has traditionally been used for treatment of various inflammatory disease including atopic dermatitis (AD). However, its action on AD is unclear. Therefore, we investigated the effect of CB on AD using NC/Nga mice as an AD model. The effect of CB on 1-Chloro-2,4-dinitrobenzene (DNCB) induced NC/Nga mice was evaluated by examining skin symptom severity, itching behavior, ear thickness, levels of serum Immunoglobulin E (IgE), tumor necrosis factor-α (TNF-α), and interleukin-4 (IL-4), skin histology. The CB significantly reduced the total clinical severity score, itching behavior, ear thickness and the level of serum IgE in AD mouse model. CB not only decreased TNF-α but also IL-4. These results suggest that CB may be a potential therapeutic modality for AD.</P>
Immunostimulatory activity of Y-shaped DNA nanostructures mediated through the activation of TLR9
Yang, Gabsik,Koo, Jung Eun,Lee, Hye Eun,Shin, Seung Won,Um, Soong Ho,Lee, Joo Young Elsevier 2019 Biomedicine & pharmacotherapy Vol.112 No.-
<P><B>Abstract</B></P> <P>Immunostimulatory oligodeoxynucleotides (DNAs) have been widely studied in pharmaceutical and biomedical research fields for applications in cancer immunotherapy and vaccination. Toll-like receptors (TLRs) are critical for the instruction and orchestration of the host immune system composed of innate and adaptive immunity. In particular, TLR9 responds to DNAs with unmethylated deoxycytosine-deoxyguanosine (CpG) motifs, thereby inducing the activation of innate immune cells, such as dendritic cells, and consequently, adaptive immune cells. In this study, we developed two kinds of Y-shaped double-stranded DNA nanostructures (Y-DNAs), including a single unit composed of three DNA strands (Y<SUB>S</SUB>-DNA) and a ligated multiunit complex formed by crosslinking each Y<SUB>S</SUB>-DNA (Y<SUB>L</SUB>-DNA), and investigated whether they have immunostimulatory activity in innate immune cells. Y<SUB>S</SUB>-DNA and Y<SUB>L</SUB>-DNA induced the production of immune cytokines such as IL-12 and TNF-α and the expression of costimulatory molecules such as CD80 and CD86 in primary mouse dendritic cells and macrophage cells (RAW264.7 cells). A Coprecipitation study demonstrated that Y<SUB>L</SUB>-DNA was directly associated with TLR9. The induction of immune cytokines by Y<SUB>S</SUB>-DNA and Y<SUB>L</SUB>-DNA was abolished in TLR9-deficient primary mouse dendritic cells. The results demonstrated that Y-DNAs induced the activation of dendritic cells and macrophages mediated by the activation of TLR9, as shown by the expression of immune cytokines and costimulatory molecules. The results suggest that Y-DNA nanostructures provide a beneficial strategy for immunotherapy by modulating the immune system.</P>
Yang, Gabsik,An, Hyo-Jin Informa Healthcare USA, Inc. 2014 IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY Vol.36 No.1
<P>The bark of <I>Sorbus commixta</I> has been used in Asian traditional medicine for treatment of cough, asthma, bronchial disorders, gastritis and dropsy. However, the anti-inflammatory effect of β-sitosteryl-3- <I>O</I> -β-glucopyranoside, a major compound of the bark of <I>S. commixta</I>, is poorly understood. In this study, we investigated the anti-inflammatory effect and the underlying molecular mechanisms of β-sitosteryl-3-O-β-glucopyranoside in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>) and cytokines released from cells were measured using EIA assay kit. The expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, Tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) was measured by real-time polymerase chain reaction (RT-PCR) and/or Western blot analysis. β-sitosteryl-3-O-β-glucopyranoside inhibited the production of nitric oxide (NO) and PGE<SUB>2</SUB> along with the expression of iNOS and COX-2 in LPS-stimulated RAW264.7 cells. In addition, β-sitosteryl-3-O-β-glucopyranoside reduced the release of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6. Moreover, β-sitosteryl-3-O-β-glucopyranoside inhibited the NF-κB activation induced by LPS, which was associated with the abrogation of IκBα degradation and subsequent decreases in nuclear p65 levels. The result suggested that the β-sitosteryl-3-<I>O</I>-β-glucopyranoside inhibited NO and pro-inflammatory productions by down-regulating the gene expression of pro-inflammatory mediators via the negative regulation of the NF-кB pathway in LPS-stimulated RAW 264.7 cells.</P>
Yang, Gabsik,Yeon, Sang Hyeon,Lee, Hye Eun,Kang, Han Chang,Cho, Yong Yeon,Lee, Hye Suk,Lee, Joo Young Oxford University Press 2018 Rheumatology Vol.57 No.4
<P>Conclusion. Oral administration of SFN effectively alleviated acute gouty inflammation by suppression of the NLRP3 inflammasome. Our results provide a novel strategy in which oral treatment with SFN may be beneficial in preventing acute attacks of gout.</P>
( Gabsik Yang ),( Seon Joo Lee ),( Han Chang Kang ),( Yong-yeon Cho ),( Hye Suk Lee ),( Christos C. Zouboulis ),( Sin-hee Han ),( Kyung-ho Ma ),( Jae-ki Jang ),( Joo Young Lee ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.5
Activation of the NLRP3 inflammasome is critical for host defense as well as the progression of inflammatory diseases through the production of the proinflammatory cytokine IL-1β, which is cleaved by active caspase-1. It has been reported that overactivation of the NLRP3 inflammasome contributes to the development and pathology of acne vulgaris. Therefore, inhibiting activation of the NLRP3 inflammasome may provide a new therapeutic strategy for acne vulgaris. In this study, we investigated whether auranofin, an anti-rheumatoid arthritis agent, inhibited NLRP3 inflammasome activation, thereby effectively treating acne vulgaris. Auranofin suppressed NLRP3 inflammasome activation induced by Propionibacterium acnes, reducing the production of IL-1β in primary mouse macrophages and human sebocytes. In a P. acnes-induced acne mouse model, injection of P. acnes into the ears of mice induced acne symptoms such as redness, swelling, and neutrophil infiltration. Topical application of auranofin (0.5 or 1%) to mouse ears significantly reduced the inflammatory symptoms of acne vulgaris induced by P. acnes injection. Topical application of auranofin led to the downregulation of the NLRP3 inflammasome activated by P. acnes in mouse ear skin. These results show that auranofin inhibits the NLRP3 inflammasome, the activation of which is associated with acne symptoms. The results further suggest that topical application of auranofin could be a new therapeutic strategy for treating acne vulgaris by targeting the NLRP3 inflammasome.
Yang, Gabsik,Lee, Hye Eun,Lim, Kyung-Min,Choi, Yong-Kyu,Kim, Kyu-Bong,Lee, Byung-Mu,Lee, Joo Young Elsevier 2018 Chemico-biological interactions Vol.284 No.-
<P><B>Abstract</B></P> <P>Certain cosmetic colorants are irritant to skin or aggravate dermatitis. Thymic stromal lymphopoietin (TSLP) plays an important role in the initiation and progress of skin inflammation and atopic dermatitis by triggering Th2 immune responses. However, the effects of cosmetic colorants on TSLP production are unknown yet. Therefore, we investigated whether cosmetic colorants regulated TSLP production and dermatitis. Lithol Rubine B (LR-B, Pigment Red 57) and its calcium salt (LR-BCA), commonly used cosmetic colorants, potentiated phorbol-12-myristate-13-acetate-induced TSLP production in keratinocytes. In addition, the topical exposure to LR-B or LR-BCA on mouse ear upregulated a TSLP inducer (MC903)-induced TSLP production and Th2 cytokine expression. Dermatitis symptoms and serum IgE and histamine levels were also aggravated by LR-B or LR-BCA, implicating the role of increased TSLP expression in acute dermatitis. LR-B or LR-BCA induced IκBα degradation and NF-κB activation in keratinocytes, leading to TSLP expression. Collectively, our results demonstrate that LR-B and LR-BCA increase TSLP expression and Th2 immune responses, thereby aggravating acute dermatitis in the compromised skin. The results further suggest that certain cosmetic colorants such as LR-B may aggravate dermatitis under pro-inflammatory conditions by upregulating TSLP production.</P> <P><B>Highlights</B></P> <P> <UL> <LI> A cosmetic colorant, lithol Rubine B potentiated TSLP production in keratinocytes. </LI> <LI> Topical application of lithol Rubine B aggravated the dermatitis symptoms in mice. </LI> <LI> Aggravated dermatitis was linked to the increased Th2 cytokines in skin. </LI> <LI> Lithol Rubine B increases the susceptibility to dermatitis through TSLP production. </LI> </UL> </P>
Ham, Inhye,Yang, Gabsik,Lee, Jaejun,Lee, Kyung-Jin,Choi, Ho-Young Marcel Dekker 2009 IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY Vol.31 No.3
<P>Hyperlipidemia has been implicated in atherosclerosis which is the leading cause of death among world population and resulting from lipid metabolic changes is a major cause of atherosclerosis. Bambusae Caulis in Taeniam belongs to Bambusaceae is the stem of Phyllostachys nigra (Lodd.) Munro var. henonis (Bean) Stapf of Phyllostachys bambusoides Siebold et Zuccarini, the perennial evergreen tree. The green middle layer of stem is dried in string-shape I shadow after the bark had been removed. In this study, the effects of middle layer of PN, PB, PP, and BCT on rat with hyperlipidemia, induced by Triton WR-1339 and high cholesterol diet were investigated. We measured plasma levels of triglyceride, total cholesterol, low-density lipoprotein (LDL)-cholesterol, and high-density lipoprotein (HDL)-cholesterol as measure of its hyperlipidemic effects. As a result, all of the Bambusae Caulis in Taeniam was reduced total cholesterol, LDL. Inhibition rate on LDL-oxidation, hACAT-1, and hACAT-2 was increased dose-dependently. Therefore all of the Bambusae Caulis in Taeniam is a good candidate for the treatment on Triton WR-1339 and high cholesterol diet-induced blood circulatory disorders, obesity, and hyperlipidemia.</P>