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( Xian Li ),( Ju Hye Yang ),( Ye Jin ),( Fansi Jin ),( Dong Young Kim ),( Jae Hoon Chang ),( Jung Ae Kim ),( Jong Keun Son ),( Tae Chul Moon ),( Kun Ho Son ),( Hyeun Wook Chang ) 영남대학교 약품개발연구소 2015 영남대학교 약품개발연구소 연구업적집 Vol.25 No.-
Ethnopharmacological relevance: 15,16-Dihydrotanshinone I (DHT-I), isolated from the dried root of Salvia miltiorrhiza Bung, which is traditionally used to treat cardiovascular and inflammatory diseases agent in Chinese medicine. DHT-I has been reported to have a broad range of biological activities, including antibacterial activity, and has been used to treat circulatory disorders, hepatitis, inflammation, cancer, and neurodegenerative diseases. Aim of the study: The aim of this study was to evaluate the anti-allergic inflammatory effects of DHT-I on degranulation and on the generation of eicosanoids, such as, prostaglandin D2 (PGD2) and leukotriene C4 (LTC4), in IgE/Ag-stimulated bone marrow-derived mast cells (BMMCs). Materials and methods: The anti-allergic inflammatory activity of DHT-I was evaluated using BMMCs. The effects of DHT-I on mast cell activation were investigated by following degranulation and eicosanoid generation using ELISA and immunoblotting and immunoprecipitation techniques. Results: DHT-I at a concentration of 20 μM markedly inhibited degranulation and the generation of PGD2 and LTC4 in IgE/Ag-stimulated BMMCs (about 90% inhibitions, respectively). Analyses of FcεRI-mediated signaling pathways demonstrated that DHT-I inhibited the phosphorylations of spleen tyrosine kinase (Syk) and linker for activation of T cells (LAT), and inhibited downstream signaling process, including [Ca2þ]i mobilization induced by the phosphorylation of phospholipase Cγ1 (PLCγ1), and the activations of mitogen-activated protein kinases (MAPKs) and the Akt-nuclear factor-κB (NF-κB) pathway. Conclusions: DHT-1 inhibits the release of allergic inflammatory mediators from IgE/Ag-stimulated mast cells by suppressing a FcεRI-mediated Syk-dependent signal pathway. This result suggests DHT-I offers a novel developmental basis for drugs targeting allergic inflammatory diseases. & 2015 Elsevier Ireland Ltd. All rights reserved.
Li, Xian,Park, Soon Jin,Jin, Fansi,Deng, Yifeng,Yang, Ju Hye,Chang, Jae-Hoon,Kim, Dong-Young,Kim, Jung-Ae,Lee, Youn Ju,Murakami, Makoto,Son, Kun Ho,Chang, Hyeun Wook Pergamon Press 2018 Biochemical pharmacology Vol.152 No.-
<P><B>Abstract</B></P> <P>AMP-activated protein kinase (AMPK) and its upstream mediators liver kinase B1 (LKB1) and sirtuin 1 (Sirt1) are generally known as key regulators of metabolism. We have recently reported that the AMPK pathway negatively regulates mast cell activation and anaphylaxis. Tanshinone IIA (Tan IIA), an active component of <I>Salvia miltiorrhiza</I> extract that is currently used for the treatment of cardiovascular and cerebrovascular diseases, shows anti-diabetic activity and improves insulin resistance in <I>db/db</I> mice through activation of AMPK. The aim of this study was to evaluate the anti-allergic activity of Tan IIA <I>in vivo</I> and to investigate the underlying mechanism <I>in vitro</I> in the context of AMPK signaling. The anti-allergic effect of Tan IIA was evaluated using mouse bone marrow-derived mast cells (BMMCs) from <I>AMPKα2</I> <SUP>−/−</SUP> or <I>Sirt1</I> <SUP>−/−</SUP> mice, or BMMCs transfected with siRNAs specific for AMPKα2, LKB1, or Sirt1. <I>AMPKα2</I> <SUP>−/−</SUP> and <I>Sirt1</I> <SUP>−/−</SUP> mice were used to confirm the anti-allergic effect of Tan IIA in anaphylaxis <I>in vivo</I>. Tan IIA dose-dependently inhibited FcεRI-mediated degranulation and production of eicosanoids and cytokines in BMMCs. These inhibitory effects were diminished by siRNA-mediated knockdown or genetic deletion of AMPKα2 or Sirt1. Moreover, Tan IIA inhibited a mast cell-mediated local passive anaphylactic reaction in wild-type mice, but not in <I>AMPKα2</I> <SUP>−/−</SUP> or <I>Sirt1</I> <SUP>−/−</SUP> mice. In conclusion, Tan IIA suppresses FcεRI-mediated mast cell activation and anaphylaxis through activation of the inhibitory Sirt1-LKB1-AMPK pathway. Thus, Tan IIA may be useful as a new therapeutic agent for mast cell-mediated allergic diseases.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Two New Species of The Genus Tmarus(Araneae, Thomisidae) from China
Yin Chang Min, Peng Xian-Jin, Gong Lian Su, 김주필(Joo Pil Kim) 한국거미연구소 2004 한국거미 Vol.20 No.1
게거미과의 중국산 신종인 Tmarus yani와 Tmarus gongi을 보고하고자 한다. The present paper deals with two new species, Tmarus yani sp. novo and Tmarus gongi sp. nov., from China. Type specimens are deposited at College of Life Sciences, Hunan Normal University. Measurements are in millimeter.
One New Secies of The Genus Borboropactus(Araneae, Thomisidae) from China
Yin Chang-Min, Peng Xian-Jin, Yan Hen-Mei, 김주필(Joo Pil Kim) 한국거미연구소 2004 한국거미 Vol.20 No.1
게거미과의 중국산 신종인 Borboropactus jiangyong을 보고하고자 한다. The present paper reports one new species, Borboropactus jiangyong sp. nov., from China. Type specimen is deposited at College of Life Sciences, Hunan Normal University. Measurements are in millimeter.
One New Species of The Genus Phrynarachne(Araneae, Thomisidae) from China
Peng Xian-Jin, Yin Chang Min, 김주필(Joo Pil Kim) 한국거미연구소 2004 한국거미 Vol.20 No.1
게거미과의 중국산 신종인 Phrynarachne sinensis을 보고하고자 한다. The present paper reports one new species, Phrynarachne sinensis sp. nov., from China. Type specimen is deposited at College of Life Sciences, Hunan Normal University. Measurements are in millimeter.
( Seung Lark Hwang ),( Yong Tae Jeong ),( Xian Li ),( Yong Deuk Kim ),( Yue Lu ),( Young Chae Chang ),( In Kyu Lee ),( Hyeun Wook Chang ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
BACKGROUND AND PURPOSE: Endoplasmic reticulum (ER) stress has been implicated in the pathogeneses of insulin resistance and type 2 diabetes, and extracellular signal-regulated kinase (ERK) antagonist is an insulin sensitizer that can restore muscle insulin responsiveness in both tunicamycin-treated muscle cells and type 2 diabetic mice. The present study was undertaken to determine whether the chemical or genetic inhibition ER stress pathway targeting by ERK results in metabolic benefits in muscle cells. EXPERIMENTAL APPROACH: ER stress was induced in L6 myotubes using tunicamycin (5 μg·mL(-1) ) or thapsigargin (300 nM) and cells were transfected with siRNA ERK or AMPKα2. Changes in ER stress and in the ERK and AMPK signalling pathways were explored by Western blotting. The phosphorylation levels of insulin receptor substrate 1 were analysed by immunoprecipitation and using glucose uptake assay. KEY RESULTS: ER stress dampened insulin-stimulated signals and glucose uptake, whereas treatment with the specific ERK inhibitor U0126 (25 μM) rescued impaired insulin signalling via AMPK activation. In db/db mice, U0126 administration decreased markers of insulin resistance and increased the phosphorylations of Akt and AMPK in muscle tissues. CONCLUSIONS AND IMPLICATIONS: Inhibition of ERK signalling pathways by a chemical inhibitor and knockdown of ERK improved AMPK and Akt signallings and reversed ER stress-induced insulin resistance in L6 myotubes. These findings suggest that ERK signalling plays an important role in the regulation of insulin signals in muscle cells under ER stress. Abbreviations: ACC, acetyl-CoA carboxylase; Ad-DN-AMPK adenovirus dominat negative; AMPK, AMP-activated protein kinase; ER, endoplasmic reticulum; PERK, RNA-activated protein kinase-like ER resident kinase; IRE-1, inositol-requiring kinase-;siRNA, small interfering RNA; UPR, unfolded protein; IRS-1, insulin receptor substrate-1; WT, wild type
( Seung Lark Hwang ),( Ju Hye Yang ),( Yong Tae Jeong ),( Yong Deuk Kim ),( Xian Li ),( Yue Lu ),( Young Chae Chang ),( Kun Ho Chang ),( Kun Ho Son ),( Hyeun Wook Chang ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0
The aim of the present study was to determine the effect of Tanshinone IIA (Tan IIA) on endoplasmic reticulum (ER) stress-induced insulinresistance in L6 myotubes and db/db mice. ER stress markers, RNA-activated protein kinase-like ER resident kinase (PERK), JNK, and AMPK activity were determined in tunicamycin-treated L6 myotubes. Insulin resistance was monitored using glucose uptake assays in vitro and blood glucose levels in vivo. Tan IIA clearly suppressed the phosphorylations of PERK and JNK and potentiated insulin-mediated Akt phosphorylation as well as glucose uptake via AMPK activation under ER stress. Furthermore, these effects are completely abrogated by siRNA-mediated knockdown of AMPK or LKB1. In addition, Tan IIA reduced blood glucose levels and body weights in db/db mice without altering food intake. These findings suggest that Tan IIA enhances insulin sensitivity and improves glucose metabolic disorders by increasing AMPK activity and attenuating ERstress-induced insulin resistance. ⓒ2012 Elsevier lnc. All rights reserved.
( Xian Li ),( Yue Lu ),( Ye Jin ),( Jong Keun Son ),( Seung Ho Lee ),( Hyeun Wook Chang ) 한국응용약물학회 2014 Biomolecules & Therapeutics(구 응용약물학회지) Vol.22 No.1
Curcumin is naturally occurring polyphenolic compound found in turmeric and has many pharmacological activities. The present study was undertaken to evaluate anti-allergic inflammatory activity of curcumin, and to investigate its inhibitory mechanisms in immunoglobulin E (IgE)/Ag-induced mouse bone marrow-derived mast cells (BMMCs) and in a mouse model of IgE/Ag-mediated passive systemic anaphylaxis (PSA). Curcumin inhibited cyclooxygenase-2 (COX-2) dependent prostaglandin D2 (PGD2) and 5-lipoxygenase (5-LO) dependent leukotriene C4 (LTC4) generation dose-dependently in BMMCs. To probe the mechanism involved, we assessed the effects of curcumin on the phosphorylation of Syk and its downstream signal molecules. Curcumin inhibited intracellular Ca2+ influx via phospholipase Cγ1 (PLCγ1) activation and the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor-κB (NF-κB) pathway. Furthermore, the oral administration of curcumin significantly attenuated IgE/Ag-induced PSA, as determined by serum LTC4, PGD2, and histamine levels. Taken together, this study shows that curcumin offers a basis for drug development for the treatment of allergic inflammatory diseases.