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RISS 인기검색어
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- 저자 : ( Xiu Mei Che ) (검색결과 2 건)
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( Soo Jung Park ),( Ki Cheong Park ),( You Hyun Kang ),( Hyun A Jin ),( Xiu Mei Che ),( Seung Won Kim ),( Sung Pil Hong ),( Tae Il Kim ),( Won Ho Kim ),( Jae Hee Cheon ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Triggering receptor expressed on myeloid cells (TREM)-1 constitutively expressed in macrophage, and upregulated by bacterial components, such as lipopolysaccharide (LPS), and functions as an amplifying molecule in infi ammatory responses. Recent studies have reported that TREM-1 expression is up-regulated in patients with infi ammatory bowel disease (IBD). In this study, we expected that guggulsterone (GGS) functions as reducer of TREM-1 in macrophage and investigated the anti-infi ammatory effects of GGS via the inhibition of NF-κB/TREM-1 in mononuclear cells using RAW264.7 activated by LPS and TNBS-induced colitis model of knockout mice. Methods: We are checked the mRNA level of TREM-1 and toll like receptor 4 (TLR4) using real time RT-PCR and the protein level of IκBa and phospho-IκBa using western blotting and ELISA, and nuclear translocation of NF-κB using immunofi uorescence. MG132 and TREM-1 antibody were used to determine the interaction of NF-κ B and TREM-1 signaling. Mouse colitis is induced by the administration of TNBS into the colon. Results: GGS treatment decreased the mRNA and protein levels of TREM-1, TLR4, TNF-a, IL-6, IL17, COX-2, and MMP-9 by blocking the phosphorylation and degradation of IκBa as well as nuclear translocation of NF-κB in RAW264.7 macrophage activated by LPS. In the TNBS-induced colitis model, GGS reduced disease activity index (DAI), and infi ammation related protein expressions by suppressing NF-κB and TREM- 1 activation in colon mucosa. Conclusions: GGS blocks the NF-κB signaling pathway by targeting the TREM-1 in RAW264.7 macrophage activated by LPS and TNBS-induced mouse colitis model. Ourresults provide an insight into the mutual relationship NF-κB and TREM-1 signaling pathway. Eventually, these fi ndings shows that GGS has a anti-infi ammatory effects in macrophage cells through the regulation of the TREM-1 and NF-κB signaling, which suggests that GGS is a potential therapeutic agent for the treatment of IBD.
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( Seung Won Kim ),( You Hyun Kang ),( Jin Hyun A ),( Xiu Mei Che ),( Tae Il Kim ),( Won Ho Kim ),( Jae Hee Cheon ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Currently, infi ammatory bowel disease (IBD) is considered to be caused by complex interactions of genetic, environmental, and other processes involvingimmunoregulatory factors. Given the large number of microRNAs (miRNA) annotated in the human genome, 30%-80% of human genes are predicted to be infi uenced by miRNAs. Among these miRNA, miR-146A acts as a negative feedback regulator to limit TRAF6 and IRAK1/2 mediated signaling and as amplifi er to upregulate NOD2 signaling and NO in infi ammatory settings. The aim of this study was to investigate theassociation between miRNA and the chronic infi ammation in the Korean population with IBD. Methods: Genotyping of miRNA SNPs rs2910164 (mir146A), rs6505162 (mir423), rs895819 (mir27A), rs11614913 (mir196A2), and rs3746444 (mir499) was performed in 195patients with Crohn`s disease (CD), 241 patients with ulcerative colitis (UC), and 149 healthy controls using TaqMan genotyping assays. We are checked the miRNA level and stability using TaqMan real time RT-PCR, FACS analysis, and cell imaging after transfection of miRNA into HT-29 cell, intestinal epithelial cells (IECs), or Jurkat T cell. Results: Among fi ve miRNA, only miR-146A SNP, rs2910164, is signifi cantly correlated patients with UC [P < 0.009 OR: 1.75 (1.14-2.67) in dominant model]. miR-146A-G (miR-146A with G allele) displayed increased stability compared with miR-146A-C. miR-146A suppressed the proliferation of HT-29 cell via suppression of EGF signaling, whereas miR-146A increased the proliferation of Jurkat T cell. Conclusions: We have identifi ed the correlation between the variation of miR-146A and UC that established different mechanism between immune cell and IECs. novel molecular regulators identifi ed in the current study would thus serve the possibility of developing better regime to treat IBD pathophysiology.
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