Mechanism of action of disease modifying anti-rheumatic agent, gold sodium thiomalate (GSTM)

Mangalam, Ashutosh K. ; Aggarwal, Amita ; Naik, Sita (2001) Mechanism of action of disease modifying anti-rheumatic agent, gold sodium thiomalate (GSTM) International Immunopharmacology, 1 (6). pp. 1165-1172. ISSN 1567-5769

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GSTM has been used for long in the treatment of rheumatoid arthritis (RA). However, its mechanism of action is still poorly understood. In the last decade, tumor necrosis factor-α (TNF- α) has emerged as the major pro-inflammatory cytokine in the pathogenesis of RA. We studied the effect of GSTM on spontaneous and LPS-stimulated TNF- α production by human peripheral blood mononuclear cells (PBMCs) of normal volunteers. PBMCs were isolated from 20 normal volunteers and cultured in the presence or absence of lipopolysaccharide (LPS 10 ng/ml) and GSTM (1 μ g/ml). TNF-α level was measured using commercial enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR). The TNF-α response to LPS was heterogeneous. PBMCs of 24 subjects showed high LPS-stimulated TNF-α production (LPS-responsive group), whereas that of six individuals had low LPS-stimulated TNF- α production (LPS-non-responsive group). GSTM-stimulated spontaneous TNF- α production and inhibited LPS-stimulated TNF-α production in 16 of 24 (75%) individuals of LPS-responsive group and one of six individuals (17%) of LPS-non-responsive group. The suppression of TNF-α by GSTM was also demonstrated at the mRNA level. We conclude that there is a heterogeneity among normal population for TNF-α production in response to LPS, and GSTM inhibits LPS-stimulated TNF-α production, primarily in LPS responders. Further study is needed to establish the relationship between LPS responsiveness and GSTM suppression.

Item Type:Article
Source:Copyright of this article belongs to Elsevier Science.
Keywords:Rheumatoid Arthritis; Cytokines; Tumor Necrosis Factor (TNF); Sodium Aurothiomalate; Gold Compounds
ID Code:79482
Deposited On:27 Jan 2012 13:17
Last Modified:27 Jan 2012 13:17

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