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Avicenna Journal of Medical Biotechnology، جلد ۹، شماره ۱، صفحات ۸-۱۲
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| عنوان فارسی |
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| چکیده فارسی مقاله |
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| کلیدواژه‌های فارسی مقاله |
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| عنوان انگلیسی |
The Role of M2000 as an Anti-inflammatory Agent in Toll-Like Receptor 2/microRNA-155 Pathway |
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| چکیده انگلیسی مقاله |
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 autoimmune and inflammatory diseases. |
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| کلیدواژه‌های انگلیسی مقاله |
MicroRNAs, SHIP1, SOCS1 |
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| نویسندگان مقاله |
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| نشانی اینترنتی |
http://www.ajmb.org/En/Article.aspx?id=260 |
| فایل مقاله |
اشکال در دسترسی به فایل - ./files/site1/rds_journals/133/article-133-376022.pdf |
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| زبان مقاله منتشر شده |
en |
| موضوعات مقاله منتشر شده |
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