Regular ArticleThe Effect of Sulfasalazine on Rheumatoid Arthritic Synovial Tissue Chemokine Production☆
References (46)
- et al.
Monocyte chemoattractant protein 1 and interleukin 8 production by rheumatoid synoviocytes. Effects of anti-rheumatic drugs
Cytokine
(1994) - et al.
Cooperative interaction of nuclear factor-kappa B- and cis-regulatory enhancer binding protein-like factor binding elements in activating the interleukin-8 gene by pro-inflammatory cytokines
J. Biol. Chem.
(1990) - et al.
IL-8/NAP-1 is the major T-cell chemoattractant in synovial tissues of rheumatoid arthritis
Clin. Immunol. Immunopathol.
(1996) - et al.
Inhibition of extracellular release of proinflammatory secretory phospholipase A2 (sPLA2) by sulfasalazine: A novel mechanism of anti-inflammatory activity
Biochem. Pharmacol.
(1997) - et al.
Transcriptional regulation of the human monocyte chemoattractant protein-1 gene. Cooperation of two NF-kappaB sites and NF-kappaB/Rel subunit specificity
J. Biol. Chem.
(1997) - et al.
Expression of monocyte chemotactic and activating factor in rheumatoid arthritis
Arthritis Rheum.
(1993) The history of the use of sulphasalazine in rheumatology
Br. J. Rheumatol.
(1995)- et al.
Rheumatoid arthritis: C-reactive protein and erythrocyte sedimentation rate during initial treatment
Br. Med. J.
(1978) - et al.
Direct suppression of human synovial cell proliferation in vitro by salazosulfapyridine and bucillamine
J. Rheumatol.
(1996) - et al.
The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis
Arthritis Rheum.
(1988)
Human chemokines: An update
Annu. Rev. Immunol.
Sulphasalazine, sulphapyridine or 5-aminosalicylic acid—Which is the active moiety in rheumatoid arthritis?
Br. J. Rheumatol.
Relationship between serum RANTES levels and radiological progression in rheumatoid arthritis patients treated with methotrexate
Clin. Exp. Rheumatol.
Adenosine inhibits cytokine release and expression of adhesion molecules by activated human endothelial cells
Am. J. Physiol.
Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhibition of prostaglandin synthesis and p105 of NFkappaB
Proc. Natl. Acad. Sci. USA
Plasma and synovial fluid concentrations of sulphasalazine and two of its metabolites in rheumatoid arthritis
Rheumatol. Int.
Interleukin-8, interleukin-10, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression levels are higher in synovial tissue from patients with rheumatoid arthritis than in osteoarthritis
Scand. J. Immunol.
The anti-inflammatory mechanism of sulfasalazine is related to adenosine release at inflamed sites
J. Immunol.
Rheumatoid arthritis: Pathophysiology and implications for therapy
N. Engl. J. Med.
Selective inhibition of human neutrophil chemotaxis to N-formyl-methionyl-leucyl-phenylalanine by sulfones
J. Immunol.
Stimulation of neovascularization by human rheumatoid synovial tissue macrophages
Arthritis Rheum.
Functional heterogeneity of human rheumatoid synovial tissue macrophages
J. Rheumatol.
Cited by (36)
Synthesis of Fe<inf>3</inf>O<inf>4</inf>-SiO<inf>2</inf>@ZnO nanocomposite: A RSM study towards sulfasalazine photodegradation
2024, Inorganic Chemistry CommunicationsAnti-rheumatoid drugs advancements: New insights into the molecular treatment of rheumatoid arthritis
2022, Biomedicine and PharmacotherapyCitation Excerpt :The action of sulfasalazine may be due to its ability to increase adenosine synthesis at the site of inflammation, inhibit the TNF-α expression, and to suppress B-cell function. Moreover, it was reported that sulfapyridine could also reduce IL-8 production [55]. Sulfasalazine is generally considered to be safe, however some adverse effects are related to its utilization, among of which, renal injury, leukopenia and agranulocytosis, central nervous system toxicity, and infertility [54,56,57].
Effects of salazosulfapyridine on the profile of cell surface proteins, revealed by biotinylation of cell surface proteins and 2-dimentional electrophoresis
2019, Biochimica et Biophysica Acta - Proteins and ProteomicsCitation Excerpt :5ASA inhibits proliferation of T cells by suppression of IL-2 production [5]. SP inhibits production of IL-8, chemokine (C-X-C motif) ligand 1 (CXCL1), and monocyte chemotactic protein-1 (MCP-1) in synovial cells from patients with rheumatoid arthritis (RA) [6]. Thereby orally administrated SASP is thought to show anti-rheumatic functions through the forms of SASP, SP, and 5ASA.
Pharmacotherapy Pearls in Rheumatology for the Care of Older Adult Patients: Focus on Oral Disease-Modifying Antirheumatic Drugs and the Newest Small Molecule Inhibitors
2018, Rheumatic Disease Clinics of North AmericaCitation Excerpt :SSZ is composed of sulfapyridine and 5-aminosalicylic acid and it is thought that the antiarthritic activity of this compound is mostly conferred by the sulfapyridine moiety. The precise mechanism of action of SSZ is not elucidated but may involve several anti-inflammatory and immunomodulatory effects, such as inhibition of proinflammatory cytokines (eg, TNF-α and IL-8) and increase of adenosine release at inflamed sites (similar to MTX).81–83 Genetic polymorphisms may play a role in the efficacy of the drug and the propensity for adverse effects.
Photodegradation of sulfasalazine and its human metabolites in water by UV and UV/peroxydisulfate processes
2018, Water ResearchCitation Excerpt :The widespread occurrence of pharmaceuticals and their metabolites in natural waters has recently received growing public and regulatory attention considering their potential adverse effects on human health and ecological systems (Kümmerer, 2009; Celiz et al., 2009; La Farré et al., 2008; Bonvin et al., 2012). Sulfasalazine (SSZ), also known as azulfidine, is a medicine widely prescribed for treatment of inflammatory bowel disease (e.g., ulcerative colitis and Crohn's disease) as well as rheumatoid arthritis (Volin et al., 2002). SSZ is a conjugate of sulfapyridine (SPD) and 5-aminosalicylic acid (5-ASA) linked by an azo bond (see Fig. 1 for molecular structures).
Desirable and Adverse Effects of Antiinflammatory Agents on the Heart
2017, The Heart in Rheumatic, Autoimmune and Inflammatory Diseases: Pathophysiology, Clinical Aspects and Therapeutic Approaches
- ☆
Preliminary results were presented as part of the 64th National Meeting of the American College of Rheumatology.