M2000作为抗炎剂在Toll样受体2/微小RNA-155通路中的作用
The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway.
作者信息
Pourgholi Fatemeh, Hajivalili Mahsa, Razavi Rasoul, Esmaeili Shadi, Baradaran Behzad, Movasaghpour Ali Akbar, Sadreddini Sanam, Goodarzynejad Hamidreza, Mirshafiey Abbas, Yousefi Mehdi
机构信息
Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Hematology and Blood Banking, Tarbiat Modares University, Tehran, Iran.
出版信息
Avicenna J Med Biotechnol. 2017 Jan-Mar;9(1):8-12.
BACKGROUND
M2000 is a newly designed and safe Non-Steroidal Anti-Inflammatory Drug (NSAID). The aim of this study was to assess the effects of M2000 on expression levels of Suppressor of Cytokine Signaling-1 (SOCS-1) and Src Homology-2 domain-containing inositol-5'-phosphatase 1 (SHIP1) proteins Toll-Like Receptor (TLR) 2/microRNA-155 pathway.
METHODS
HEK293 TLR2 cell line and Peripheral Blood Mononuclear Cells (PBMCs) were treated by different concentrations of M2000 in MTT assay. RNA was extracted by miRNeasy Mini kit. Then, cDNA was synthesized and the expression levels of SOCS1, SHIP1 and miRNA155 were evaluated by Quantitative Real time PCR.
RESULTS
Our results showed that M2000 significantly increased the expression levels of SOCS1 and SHIP-1 in Lipopolysachride (LPS)-treated and non-treated cells. Moreover, M2000 decreased expression level of miR-155 in LPS treated PBMCs.
CONCLUSION
M2000 can be used as NSAID in LPS induced inflammation and decrease inflammatory cytokines production by targeting SOCS1, SHIP1 and miR-155 in auto-immune and inflammatory diseases.
背景
M2000是一种新设计的安全非甾体抗炎药（NSAID）。本研究的目的是评估M2000对细胞因子信号转导抑制因子1（SOCS-1）和含Src同源2结构域的肌醇-5'-磷酸酶1（SHIP1）蛋白以及Toll样受体（TLR）2/微小RNA-155通路表达水平的影响。
方法
在MTT试验中，用不同浓度的M2000处理HEK293 TLR2细胞系和外周血单核细胞（PBMCs）。用miRNeasy Mini试剂盒提取RNA。然后，合成cDNA，并通过定量实时PCR评估SOCS1、SHIP1和miRNA155的表达水平。
结果
我们的结果表明，M2000显著提高了脂多糖（LPS）处理和未处理细胞中SOCS1和SHIP-1的表达水平。此外，M2000降低了LPS处理的PBMCs中miR-155的表达水平。
结论
在自身免疫性和炎性疾病中，M2000可作为NSAID用于LPS诱导的炎症，并通过靶向SOCS1、SHIP1和miR-155减少炎性细胞因子的产生。
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