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The Role of M2000 As an Anti-Inflammatory Agent in Toll-Like Receptor 2/Microrna-155 Pathway



Pourgholi F1, 2, 3 ; Hajivalili M1, 2, 3 ; Razavi R4 ; Esmaeili S4 ; Baradaran B2, 3 ; Movasaghpour AA1, 3 ; Sadreddini S2 ; Goodarzynejad H5 ; Mirshafiey A6 ; Yousefi M2, 3
Authors
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Authors Affiliations
  1. 1. Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
  2. 2. Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
  3. 3. Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
  4. 4. Department of Hematology and Blood Banking, Tarbiat Modares University, Tehran, Iran
  5. 5. Basic and Clinical Research Department, Tehran Heart Center, Tehran, Iran
  6. 6. Department of Immunology, Faculty of Public Health, Tehran University of Medical Sciences, Tehran, Iran

Source: Avicenna Journal of Medical Biotechnology Published:2017

Abstract

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 domaincontaining inositol-5’-phosphatase 1 (SHIP1) proteins via 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 autoimmune and inflammatory diseases. © 2017, Avicenna Journal of Medical Biotechnology. All rights reserved.
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