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The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway

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 vi...

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Autores principales: Pourgholi, Fatemeh, Hajivalili, Mahsa, Razavi, Rasoul, Esmaeili, Shadi, Baradaran, Behzad, Movasaghpour, Ali Akbar, Sadreddini, Sanam, Goodarzynejad, Hamidreza, Mirshafiey, Abbas, Yousefi, Mehdi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Avicenna Research Institute 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5219823/
https://www.ncbi.nlm.nih.gov/pubmed/28090274
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author Pourgholi, Fatemeh
Hajivalili, Mahsa
Razavi, Rasoul
Esmaeili, Shadi
Baradaran, Behzad
Movasaghpour, Ali Akbar
Sadreddini, Sanam
Goodarzynejad, Hamidreza
Mirshafiey, Abbas
Yousefi, Mehdi
author_facet Pourgholi, Fatemeh
Hajivalili, Mahsa
Razavi, Rasoul
Esmaeili, Shadi
Baradaran, Behzad
Movasaghpour, Ali Akbar
Sadreddini, Sanam
Goodarzynejad, Hamidreza
Mirshafiey, Abbas
Yousefi, Mehdi
author_sort Pourgholi, Fatemeh
collection PubMed
description 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 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 auto-immune and inflammatory diseases.
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spelling pubmed-52198232017-01-13 The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway Pourgholi, Fatemeh Hajivalili, Mahsa Razavi, Rasoul Esmaeili, Shadi Baradaran, Behzad Movasaghpour, Ali Akbar Sadreddini, Sanam Goodarzynejad, Hamidreza Mirshafiey, Abbas Yousefi, Mehdi Avicenna J Med Biotechnol Original Article 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 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 auto-immune and inflammatory diseases. Avicenna Research Institute 2017 /pmc/articles/PMC5219823/ /pubmed/28090274 Text en Copyright© 2017 Avicenna Research Institute http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Pourgholi, Fatemeh
Hajivalili, Mahsa
Razavi, Rasoul
Esmaeili, Shadi
Baradaran, Behzad
Movasaghpour, Ali Akbar
Sadreddini, Sanam
Goodarzynejad, Hamidreza
Mirshafiey, Abbas
Yousefi, Mehdi
The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway
title The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway
title_full The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway
title_fullStr The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway
title_full_unstemmed The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway
title_short The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway
title_sort role of m2000 as an anti-inflammatory agent in toll-like receptor 2/microrna-155 pathway
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5219823/
https://www.ncbi.nlm.nih.gov/pubmed/28090274
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