NLRP3 INFLAMMASOME ACTIVATION IN MACROPHAGE (RAW 264.7) CELLS BY LIPOPOLISACCARIDE/NIGERICIN: REGULATORY EFFECT OF PSORALIDIN

Abstract

Psoralidin, a prenylated coumestan, has been reported its anti-inflammatory effect, but the regulatory effects on inflammasome activation and pyroptosis-related cytokines are not clear. The aim of this study was to investigate the regulatory role of psoralidin on inflammasome activation and expression of pyroptosis-related cytokines in Lipopolysaccharide (LPS)/Nigericin-stimulated RAW 264.7 macrophages. Regulatory mechanism of psoralidin on inflammasome activation was evaluated using Western blotting for NLRP3, adaptor protein apoptosis-associated speckle-like protein (ASC)and Caspase-1. Pyroptosis-related cytokines were evaluated using RT-PCR for interleukin-1β (IL-1β)and interleukin-18 (IL18).Non-cytotoxic concentration of Psoralidin (5.0µM) significantly inhibited LPS/Nigericin induced inflamasome activation. In addition, pretreatment with psoralidin suppressed the LPS/Nigericin-induced production of IL-1β and IL18. Our results indicate that the regulatory effects of psoralidin on inflammasome activation and pyroptosis related cytokine production in RAW 264.7 macrophages are associated with suppression of NLRP3inflammasome activation and inhibition of the release of pyroptosis related cytokines.According to these results, Psoralidine may be considered as a potential therapeutic candidate for the prevention of inflammatory diseases or to support the treatment of inflammation.