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d mannuronic acid/التهاب

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مقالاتالتجارب السريريةبراءات الاختراع
الصفحة 1 من عند 44 النتائج
Rheumatoid arthritis (RA) is the most common form of chronic inflammatory arthritis characterized by pain, swelling and destruction of joints, with a resultant disability. Disease-modifying anti-rheumatic drugs (DMARDs) and biological drugs can interfere with the disease process. In this study, the

Immunomodulatory effects of M2000 (β-D-Mannuronic acid) on TNF-α, IL-17 and FOXP3 gene expression in patients with inflammatory bowel disease.

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BACKGROUND Inflammatory bowel diseases (IBD) are immune-mediated disorders that result from an aberrant immunological response to the gut luminal antigen in genetically susceptible patients. IBD is categorized into two serotype, Crohn's diseases (CD) and ulcerative colitis (UC), both subtype are

Influence of β-D-mannuronic acid, as a new member of non-steroidal anti-inflammatory drugs family, on expression pattern of chemokines and their receptors in rheumatoid arthritis.

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Based on the encouraging results of phase III clinical trial of β-D-mannuronic acid (M2000) (as a new anti-inflammatory drug) in patients with RA, in this study, we aimed to evaluate the effects of this drug on the expression of chemokines and their receptors in PBMCs of RA

Efficacy of β-D-mannuronic acid [M2000] on pro-apoptotic process and inflammatory related molecules NFҡB, IL-8 and Cd49d using healthy donor PBMC.

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This investigation evaluates the pro-apoptotic and anti-inflammatory effects of β-D-mannuronic acid [M2000] compared to diclofenac, based on gene expression involved in apoptosis and inflammation process [including Bcl2, NFκB, IL-8 and Cd49d] in peripheral blood mononuclear cells [PBMCs] of healthy
Context: miR-146a, its targets (IRAK1, TRAF6) and NF-κB transcription factor play a fundamental role in rheumatoid arthritis (RA). Positive effects of drug β-d-mannuronic acid (M2000) were proven on their expression in the HEK-Blue hTLR2 cell line, and results of its phase III clinical trial

Pharmacological effects of β-d-mannuronic acid (M2000) on miR-146a, IRAK1, TRAF6 and NF-κB gene expression, as target molecules in inflammatory reactions.

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BACKGROUND Impaired expression and function of microRNAs (miRNAs) are involved in the pathogenesis of many autoimmune and inflammatory diseases. Moreover, there is a close relationship between TLRs and miRNAs and impairment in regulating their expression which can play a vital role in the

Pharmacological effects of β-D-mannuronic acid (M2000) on miR-146a, IRAK1, TRAF6 and NF-κB gene expression, as target molecules in inflammatory reactions.

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Impaired expression and function of microRNAs (miRNAs) are involved in the pathogenesis of many autoimmune and inflammatory diseases. Moreover, there is a close relationship between TLRs and miRNAs and impairment in regulating their expression which can play a vital role in the

Anti-diabetic effect of β-D-mannuronic acid (M2000) as a novel NSAID with immunosuppressive property on insulin production, blood glucose, and inflammatory markers in the experimental diabetes model.

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This research aimed to evaluate the anti-diabetic effects of β-d-mannuronic acid (M2000) on blood glucose, insulin production, and inflammatory markers in streptozotocin-induced diabetic rats. Our data showed that the final fasting serum glucose level was significantly lower in the M2000-treated

Immunotherapeutic Effects of β-D Mannuronic Acid on IL-4, GATA3, IL-17 and RORC Gene Expression in the PBMC of Patients with Inflammatory Bowel Diseases.

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Inflammatory bowel diseases (IBD) are chronic relapsing immune-mediated disorders that result from an aberrant immunological response. IBD comprises of Crohn's disease (CD) and ulcerative colitis (UC). The precise aetiology of IBD has not been fully understood, however, recent studies support the

Preclinical assessment of β-d-mannuronic acid (M2000) as a non-steroidal anti-inflammatory drug.

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BACKGROUND β-d-Mannuronic acid (M2000) has shown its therapeutic effects with the greatest tolerability and efficacy in various experimental models such as experimental autoimmune encephalomyelitis (EAE), adjuvant induced arthritis (AIA), nephrotic syndrome, and acute glomerulonephritis. Despite

Anti-inflammatory Property of β-D-Mannuronic Acid (M2000) on Expression and Activity of Matrix Metalloproteinase-2 and -9 through CD147 Molecule in Phorbol Myristate Acetate-differentiated THP-1 Cells.

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The aim of this study was to evaluate the effects of M2000, a novel non-steroidal anti-inflammatory drug (NSAID) with immunosuppressive property and without gastro-nephrotoxicitic effects on matrix metalloproteinases (MMP)-2 and (MMP)-9 in phorbol myristate acetate (PMA)-differentiated THP-1 cells.

The Safety Property of β-D-Mannuronic Acid (M2000) as a Novel Immunosuppressive Agent on Differentiation, Maturation and Function of Human Dendritic Cells.

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The study's background and aim: In this investigation, the safety property of M2000 (β-D-mannuronic acid) on differentiation, maturation and function of dendritic cells, was determined. β-D-mannuronic acid, as a novel immunosuppressive and anti-inflammatory agent, has been tested in various

A randomized, controlled, phase II clinical trial of β-D-mannuronic acid (M2000) in pre-surgical breast cancer patients at early stage (T1-T2).

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Following the potent efficacy of β-D-Mannuronic acid in a breast cancer murine model, we evaluated the efficacy of this novel non-steroidal anti-inflammatory drug in breast cancer patients in the present clinical trial. The study was an 8-week randomized, controlled, phase II clinical trial (IRCT:

The Biology of β-D-mannuronic acid (M2000) on Human Dendritic Cell Based on MicroRNA-155 and MicroRNA-221.

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BACKGROUND The aim of this study was to evaluate the effect of ß-Dmannuronic acid (M2000) on related miRNAs to dendritic cells (DCs) differentiation. DC-based immunosuppressive drugs can suppress the progression of autoimmune diseases, however, their notable side effects in increasing the risk of

Targeting of crosstalk between tumor and tumor microenvironment by β-D mannuronic acid (M2000) in murine breast cancer model.

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Metastasis is the main cause of death in breast cancer patients. Inflammatory processes following crosstalk between tumor cells and tumor microenvironment play an important role in progression and metastasis of cancer. Hence, targeting of these interactions may represent a novel promising strategy
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