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Oh, Jaemin,Hur, Jungmu,Kim, Yourim,Kwon, Young-Mi,Kim, Kyungsuk,Chung, Yeuntai,Choi, Minkyu Korean Society of ToxicologyKorea Environmental Mu 2004 Toxicological Research Vol.20 No.4
Background: Crohn's disease is characterized by a chronic relapsing inflammation of the bowel. Gliotoxin has been known to play strong immunosuppressive properties, while mechanisms for its anti-inflammatory actions are not completely understood. Here, we investigated the effects of gliotoxin in trinitrobenzene sulfonic acid (TNBS) induced mouse colitis, an animal model of Crohn's disease. Results: Gliotoxin dramatically improved clinical and histopathological symptoms in accompanied with reduced expression of TNF-$\alpha$, IL-1$\beta$, and ICAM-1 protein levels in TNBS induced colitis. Interestingly Gliotoxin induced Heme oxygenase-1 (HO-1) and the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) completely mimicked the protective effects of gliotoxin in TNBS induced colitis mice. In contrast, the HO-1 inhibitor zinc protoporphyrin IX (ZnPPIX) could reverse the anti-inflammatory effects of gliotoxin and CoPPIX. Conclusions: Gliotoxin is a potential therapeutic agent targeting for the treatment of Crohn's disease by inducing HO-1.
Jaemin Oh,Jungmu Hur,Yourim Kim,Young-Mi Kwon,Kyungsuk Kim,Yeuntai Chung,Minkyu Choi 한국독성학회 2004 Toxicological Research Vol.20 No.4
Crohn’s disease is characterized by a chronic relapsing inflammation of the bowel. Gliotoxin has been known to play strong immunosuppressive properties, while mechanisms for its anti-inflammatory actions are not completely understood. Here, we investigated the effects of gliotoxin in trinitrobenzene sulfonic acid (TNBS) induced mouse colitis, an animal model of Crohn’s disease. Results: Gliotoxin dramatically improved clinical and histopathological symptoms in accompanied with reduced expression of TNF-α, IL-1β, and ICAM-1 protein levels in TNBS induced colitis. Interestingly Gliotoxin induced Heme oxygenase-1 (HO-1) and the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) completely mimicked the protective effects of gliotoxin in TNBS induced colitis mice. In contrast, the HO-1 inhibitor zinc protoporphyrin IX (ZnPPIX) could reverse the antiinflammatory effects of gliotoxin and CoPPIX. Conclusions: Gliotoxin is a potential therapeutic agent targeting for the treatment of Crohn’s disease by inducing HO-1.
Kang Hyeona,Oh Yourim,Nam Keun Lee,이진규 한국미생물·생명공학회 2022 Journal of microbiology and biotechnology Vol.32 No.12
In this study, we investigated the optimal conditions for 3D structure printing of alternative fats that have the textural properties of lard using beeswax (BW)-based oleogel by a statistical analysis. Products printed with over 15% BW oleogel at 50% and 75% infill level (IL) showed high printing accuracy with the lowest dimensional printing deviation for the designed model. The hardness, cohesion, and adhesion of printed samples were influenced by BW concentration and infill level. For multi-response optimization, fixed target values (hardness, adhesiveness, and cohesiveness) were applied with lard printed at 75% IL. The preparation parameters obtained as a result of multiple reaction prediction were 58.9% IL and 16.0% BW, and printing with this oleogel achieved fixed target values similar to those of lard. In conclusion, our study shows that 3D printing based on the BW oleogel system produces complex internal structures that allow adjustment of the textural properties of the printed samples, and BW oleogels could potentially serve as an excellent replacement for fat.
Park, Hyun Ah,Lee, Jae-Won,Kwon, Ok-Kyoung,Lee, Gilhye,Lim, Yourim,Kim, Jung Hee,Paik, Jin-Hyub,Choi, Sangho,Paryanto, Imam,Yuniato, Prasetyawan,Kim, Doo-Young,Ryu, Hyung Won,Oh, Sei-Ryang,Lee, Seung Spandidos Publications 2017 International journal of molecular medicine Vol.40 No.5
<P>Physalis peruviana L. (PP) is a medicinal herb that has been confirmed to have several biological activities, including anticancer, antioxidant and anti-inflammatory properties. The aim of the present study was to evaluate the protective effect of PP on cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced pulmonary inflammation. Treatment with PP significantly reduced the influx of inflammatory cells in the bronchoalveolar lavage fluid (BALF) and lung of mice with CS- and LPS-induced pulmonary inflammation. PP also decreased the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in the BALF. PP effectively attenuated the expression of monocyte chemoattractant protein-1 (MCP-1) and the activation of extracellular signal-regulated kinase (ERK) in the lung. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) activation and heme oxygenase-1 (HO-1) expression were increased by PP treatment. In an in vitro experiment, PP reduced the mRNA expression of TNF-alpha and MCP-1, and the activation of ERK in CS extract-stimulated A549 epithelial cells. Furthermore, PP increased the activation of Nrf2 and the expression of HO-1 in A549 cells. These findings suggest that PP has a therapeutic potential for the treatment of pulmonary inflammatory diseases, such as chronic obstructive pulmonary disease.</P>
Lee, Jae-Won,Chun, Wanjoo,Kwon, Ok-Kyoung,Park, Hyun Ah,Lim, Yourim,Lee, Jae-Hyeon,Kim, Doo-Young,Kim, Jung Hee,Lee, Hyeong-Kyu,Ryu, Hyung Won,Oh, Sei-Ryang,Ahn, Kyung-Seop Elsevier 2018 INTERNATIONAL IMMUNOPHARMACOLOGY Vol.64 No.-
<P><B>Abstract</B></P> <P>The increase in inflammatory cytokines and chemokines is a common denominator in the pathogenesis of acute lung injury (ALI) which are involved in the influx of inflammatory cells and lung damage. The aim of the present study was to evaluate the protective effect of 3,4,5-trihydroxycinnamic acid (THC) in lipopolysaccharide (LPS)-induced ALI. THC efficiently decreased the mRNA expression of interleukin-8 (IL-8) in LPS-stimulated A549 airway epithelial cells. THC induced heme oxygenase-1 (HO-1) expression in A549 cells. THC also increased the activation of AMP-activated protein kinase (AMPK) in A549 cells and RAW264.7 macrophages. In LPS-induced ALI in mice, THC significantly suppressed neutrophil influx and monocyte chemoattractant protein-1 (MCP-1) production in the bronchoalveolar lavage fluid (BALF). THC also attenuated the levels of neutrophil elastase (NE), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the BALF and serum. In addition, THC inhibited the expressions of inducible nitric oxide synthase (iNOS) and the activation of nuclear factor-kappa B (NF-κB) in the lung. These protective effects of THC were accompanied with HO-1 induction and AMPK activation. Taken together, the present study clearly demonstrates that THC significantly attenuates the LPS-induced ALI, suggesting that THC might be a valuable therapeutic adjuvant in airway inflammatory disorders.</P> <P><B>Highlights</B></P> <P> <UL> <LI> THC reduces the mRNA expression of IL-8 in LPS-stimulated A549 airway epithelial cells. </LI> <LI> THC inhibits the influx of neutrophils and macrophages in the BALF of ALI mice. </LI> <LI> THC decreases the levels of NE, TNF-α and IL-6 in the BALF and serum. </LI> <LI> THC attenuates the recruitment of inflammatory cells and the production of MCP-1 in the lung. </LI> <LI> THC downregulates the activation of NF-κB and upregulates the activation of HO-1 and AMPK in the lung. </LI> </UL> </P>