2007
DOI: 10.1016/j.intimp.2007.07.020
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Bucillamine mechanism inhibiting IL-1β-induced VEGF production from fibroblast-like synoviocytes

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Cited by 15 publications
(14 citation statements)
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“…Moreover, we showed that SA981, an intramolecular disulfide form of bucillamine, inhibits the phosphorylation of Akt [14]. Therefore, Akt is thought to be an essential target of bucillamine.…”
Section: Discussionmentioning
confidence: 87%
See 1 more Smart Citation
“…Moreover, we showed that SA981, an intramolecular disulfide form of bucillamine, inhibits the phosphorylation of Akt [14]. Therefore, Akt is thought to be an essential target of bucillamine.…”
Section: Discussionmentioning
confidence: 87%
“…The results suggest that the effect of SA981 on VEGF production arises partially from inhibition of the phosphorylation of Akt and the expression of transcription factor, hypoxiainducible factor-1b (HIF-1b) and specificity protein 1 (Sp1) by IL-1b [14].…”
Section: Introductionmentioning
confidence: 99%
“…These properties of Buc and ETN may synergistically act on cytokine production in vivo. Buc also inhibits Akt signaling and vascular endothelial growth factor production [18]. In contrast, ETN inhibits TNF-a and TNF-b.…”
Section: Discussionmentioning
confidence: 99%
“…The antirheumatic effects of Buc may be caused by its modifying effects on the functions of lymphocytes [11][12][13] and synovial cells [14][15][16] as well as by its antioxidant effects [17]. Recent studies have shown that Buc partially inhibits Akt signaling [18,19]. We chose a dose of 30 mg/kg/day for Buc, which does not show significant inhibition of the development of arthritis as a therapeutic treatment.…”
Section: Discussionmentioning
confidence: 99%
“…The potentiation of therapeutic effects with the combination of two drugs suggests differences in the site or mechanism of action at or by which these two DMARDs exhibit anti-rheumatoid effects. According to a recent report, bucillamine suppresses IgM production by B cells [7], VEGF production by synoviocytes [8], and differentiation of monocytes into osteoclasts [9] based on a mechanism of action completely different from that of MTX or SSZ. In fact, it has been reported in two large clinical trials in European countries that combined treatment with MTX and SSZ, which have the similar mechanism of action [10,11], dose not provide a clear benefit, when compared with monotherapy using either agent [12,13].…”
Section: Introductionmentioning
confidence: 99%