Triptolide inhibits the inflammatory activities of neutrophils to ameliorate chronic arthritis


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Abstract

HighlightsTP alleviated AA by reducing neutrophil recruitment.TP suppressing the expression of IL-6 and TNF-α in peripheral blood of AA mice.TP suppressed the expression of pro-inflammatory cytokines in neutrophils in vitro.TP inhibited neutrophil migration and promoted neutrophil apoptosis in vitro.TP inhibited the NETosis and autophagy of neutrophils in vitro.Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by cellular infiltration into the joints and cartilage destruction. Neutrophils play a crucial role in the pathogenesis of RA. Triptolide (TP) is a bioactive compound derived from Tripterygium wilfordii Hook F, which has been used in folk medicine as a treatment for a variety of inflammatory disorders, including RA, for many centuries. Previous studies have shown that TP possesses anti-arthritic activity. However, the anti-arthritic mechanism of TP remains to be fully defined. In the present study, we used the adjuvant-induced arthritis (AA) murine model of RA to investigate the impact of TP on RA and neutrophil function. TP alleviated AA by reducing neutrophil recruitment and suppressing the expression of interleukin-6 and tumour necrosis factor-α in vivo. TP also suppressed the expression of pro-inflammatory cytokines in neutrophils, promoted neutrophil apoptosis and inhibited the migration, NETosis and autophagy of neutrophils in vitro. Based on our findings, TP effectively ameliorates RA by down-regulating neutrophil inflammatory functions, indicating that TP represents a potential therapeutic agent for RA.

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