Avicenna J Med Biotech arij002 Avicenna Journal of Medical Biotechnology 2008-2835 2008-4625 Avicenna Research Institute ajmb260 The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway PourgholiFatemehDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, IranHajivaliliMahsaDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, IranRazaviRasoulDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, IranEsmaeiliShadiDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, IranBaradaranBehzadDepartment of Biotechnology, College of Science, University of Tehran, Tehran, IranMovasaghpourAli AkbarDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, IranSadreddiniSanamInstitute of Industrial and Environmental Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, IranGoodarzynejadHamidrezaDepartment of Biology, Payame-Noor University, Tehran, IranMirshafieyAbbasReproductive Biotechnology Research Center, Avicenna Research Institute, ACECR , Tehran, IranYousefiMehdiReproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran 9 1 8 12 16 3 2016 16 5 2016

<p>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&rsquo;-phosphatase 1 (SHIP1) proteins <em>via</em> Toll-Like Receptor (TLR) 2/microRNA-155 pathway.<br /> 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.<br /> 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.<br /> Conclusion: M2000 can be used as NSAID in LPS induced inflammation and decrease inflammatory cytokines production by targeting SOCS1, SHIP1 and miR-155 in autoimmune and inflammatory diseases.</p>