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Potassium chloride inhibits NLRP3. 11 / 11
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"The pretreatment of primary monocytes with MCC950, an NLRP3 inhibitor; YVAD, a caspase-1 inhibitor; or KCl, which prevents K efflux and inhibits activation of the canonical NLRP3 inflammasome [36], all resulted in a significant decrease in IL-1β release from infected primary human monocytes from multiple independent donors (Fig 1A)."
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"Amin et al. demonstrated that DMF treatment improved vascular reactivity to KCl and acetylcholine in diabetic rat aorta by suppressing the iNOS and NLRP3 inflammasome and enhancing eNOS expression [42]."
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"Experimentally, the involvement of K + efflux is determined by showing that a given activator reduces cellular K + content and that NLRP3 activation is inhibited by high (>50 mM) concentrations of ext[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Extracellular KCl, which prevents K + efflux and NLRP3 dependent caspase-1 activation, abrogated UBE2L3 depletion (XREF_FIG D)."
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"Up to 30 mM of extracellular KCl has been reported to specifically inhibit NLRP3 inflammasome but not other inflammasome pathways or general cellular signaling ."
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"Notably, the association of NLRP3 with Nek7 as well as caspase-1 activation triggered by ATP were blocked in the presence of 50 mM KCl that inhibits potassium efflux and NLRP3 activation (XREF_FIG)."
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"Raising extracellular K concentration gradually to 40 mM with 2 M KCl solution would inhibit NLRP3 activation by canonical and non-canonical activators24 with different extents."
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"Treatment with potassium chloride to inhibit the ion channel model activation of NLRP3 and a ROS inhibitor can inhibit the maturation of interleukins and caspase-1 induced by JEV [54] ."
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"However, it was difficult to judge whether the effect of KCl was due to specific inhibition of the NLRP3 inflammasome, as the same concentration of KCl also decreased the cytokine responses of NLRP3 -/- macrophages to S. pneumoniae (data not shown)."
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"High KCl is known to inhibit NLRP3 inflammasome activation and cell death by blocking K + efflux, a common trigger of NLRP3 inflammasome activation, as confirmed by the considerable reduction in released IL-1beta in the culture supernatant18, 19."
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"A similar result was obtained by treating neutrophils with extracellular KCl, which inhibits NLRP3 by blocking K + efflux (XREF_FIG and XREF_FIG)."
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