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Exploration of mechanism of the novel Arteminsinin analogue SM934 to treat systemic lupus erythematosus
Update time: 2011-05-04
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ZUO Jianping’s group from Shanghai Institute of Materia Medica,CAS has their novel investigation “Oral administration of artemisinin analogue SM934 ameliorated the lupus syndromes in MRL/lpr mice by inhibiting Th1 and Th17 cell responses”  published online on the authoritative academic journal of rheumatology research《Arthritis and Rheumatism》.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease and multifactorial pathogenesis resulted in scarcity of therapeutic approaches for SLE. Recent years, Zuo’s group screened series of novel water-soluble arteminsinin analogues with low toxicity and high bioactivity. Moreover, previous studies proved that water-soluble arteminsinin analogues could inhibit T cell activation, inhibit production of pro-inflammatory cytokines from macrophage and could treat the experimental animal model of rheumatoid arthritis(British Journal of Pharmacology, 2009).

Recently, ZUO’s group demonstrated that the novel water-soluble Artemisinin derivative SM934 exhibited promising preventive and therapeutic effects on SLE animal model MRL/lpr mice. In vitro, SM934 inhibited IFN-γ and IL-17 production from polyclonal CD4+ T cells activated by TCR-engagement and the differentiation of naive CD4+ T cells into Th1 and Th17, but not regulatory T (Treg) cells. In vivo, MRL/lpr mice treated with SM934 showed significantly ameliorated proteinuria and renal lesion, decreased levels serum anti-dsDNA antibodies and prolonged survival period. Ex vivo, SM934 treatment elevated the percentage of Treg cells; inhibited the development of Th1 and Th17 cells; impeded the comprehensive activation of STAT1, STAT3, and STAT5 proteins in splenocytes.

This study provided a new clinical application of artemisinin and its derivatives to treat human SLE. Additionally, this study demonstrated that both IFN-γ and IL-17 should contribute to the pathogenesis and remained major therapeutic targets in SLE.

 
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