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Effects of Guluronic Acid (G2013) on Ship1, Socs1 Induction and Related Molecules in Tlr4 Signaling Pathway Publisher Pubmed



Mortazavijahromi SS1, 3 ; Farazmand A1, 2 ; Motamed N1, 2 ; Navabi SS3 ; Mirshafiey A3
Authors
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Authors Affiliations
  1. 1. Department of Cellular and Molecular Biology, Kish International Campus, University of Tehran, Kish, Iran
  2. 2. School of Biology, University College of Science, University of Tehran, Tehran, Iran
  3. 3. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran

Source: International Immunopharmacology Published:2018


Abstract

Objective This research aimed to study the anti-inflammatory and immunomodulatory effects of guluronic acid (G2013) on gene expression of TLR4, MyD88, SHIP1, SOCS1, NF-κB, and assessment of the level of IL-1β as a pro-inflammatory cytokine in HEK-Blue hTLR4 cell line. Methods The cytotoxicity of G2013 was assessed by the MTT assay. The mRNA expression levels of the mentioned genes were measured by qRT-PCR. IL-1β concentration in culture media was determined using ELISA method. Results MTT assay demonstrated that G2013 (before the concentration of 125 μg/ml) had no cytotoxic effect on HEK-Blue hTLR4 cells. Our results indicated that the low and high doses of this drug could significantly reduce the gene expression of TLR4 and MyD88, as compared to the control group (p < 0.05). Moreover, it was found that the low dose of this drug could significantly increase the gene expression of SHIP1 and SOCS1, as compared to the control group (p < 0.05). Furthermore, the study findings revealed that the level of NF-κB gene expression significantly reduced, in both doses of G2013 compared to the control group (p < 0.05, p < 0.01, respectively). Our data showed that the level of IL-1β in culture media decreased by both doses of this drug in comparison to control group (p < 0.05). Conclusion This study indicates that G2013 is able to induce SHIP1, SOCS1 and reduce TLR4, MyD88, NF-κB at the level of gene expression and decrease IL-1β as a pro-inflammatory cytokine which might be recommended for reduction of inflammatory reactions. © 2018 Elsevier B.V.
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