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

Pourgholi

Fatemeh

Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Hajivalili

Mahsa

Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Razavi

Rasoul

Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Esmaeili

Shadi

Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Baradaran

Behzad

Department of Biotechnology, College of Science, University of Tehran, Tehran, Iran

Movasaghpour

Ali Akbar

Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Sadreddini

Sanam

Institute of Industrial and Environmental Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran

Goodarzynejad

Hamidreza

Department of Biology, Payame-Noor University, Tehran, Iran

Mirshafiey

Abbas

Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR , Tehran, Iran

Yousefi

Mehdi

Reproductive 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’-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>