Title of article :
The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway
Author/Authors :
Pourgholi, Fatemeh Hematology and Oncology Research Center - Tabriz University of Medical Sciences , Hajivalili, Mahsa Hematology and Oncology Research Center - Tabriz University of Medical Sciences , Razavi, Rasoul Department of Hematology and Blood Banking - Tarbiat Modares University , Esmaeili, Shadi Department of Hematology and Blood Banking - Tarbiat Modares University , Baradaran, Behzad Immunology Research Center - Tabriz University of Medical Sciences , Movasaghpour, Ali Akbar Hematology and Oncology Research Center - Tabriz University of Medical Sciences , Sadreddini, Sanam Immunology Research Center - Tabriz University of Medical Sciences , Goodarzynejad, Hamidreza Basic and Clinical Research Department - Tehran Heart Center , Mirshafiey, Abbas Department of Immunology - Faculty of Public Health - Tehran University of Medical Sciences , Yousefi, Mehdi Immunology Research Center - Tabriz University of Medical Sciences
Pages :
5
From page :
8
To page :
12
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.
Keywords :
SOCS1 , SHIP1 , MicroRNAs
Journal title :
Astroparticle Physics
Serial Year :
2017
Record number :
2423801
Link To Document :
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