IndraLab

Statements



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"NSAIDs work by blocking Cl channels, which prevents the activation of the NLRP3 inflammasome [194]."

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"Mayes-Hopfinger et al[22] revealed that decreased intracellular Cl activates the NLRP3 inflammasome, promoting an immune response by switching the proinflammatory status of a phagocyte."

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"Low extracellular Cl - levels cause ATP induced IL-1beta secretion, whereas Cl - channel blockers and high extracellular Cl - conditions inhibit NLRP3 activation."

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"Since then, studies have demonstrated that Cl - channel inhibitors, including flufenamic acid, IAA94, DIDS, and NPPB, may inhibit NLRP3, but not AIM2 or NLRC4 inflammasome activation XREF_BIBR - XREF_BIBR."

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"The most convincing data is that a class of non-steroidal anti-inflammatory drugs (NSAIDs) prevents Cl migration via inhibiting NLRP3 activation by blocking the volume-regulated anion channel (VRAC) on the plasma membrane (54)."

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"Along the same lines, depletion of extracellular Cl and K , but neither alone, suffice to activate NLRP3 in LPS primed cells (160)."

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"So, we surmised that inhibiting NLRP3 inflammasome-mediated pyroptosis will suppress AIS-induced nerve injury.The data also showed that CL treatment reversed AIS- and OGD-induced nerve injury by suppressing NLRP3/caspase-1 pathway activations."

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"More importantly, we found that IL-1β decreased the expression of Kindlin-2 and CL further downregulated Kindlin-2 and upregulated Nlrp3 and Casp1 in IL-1β treated NP cells (Fig. 4j–m)."

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"Furthermore, targeting Cl channels only inhibited K -dependent canonical NLRP3 activation."

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"In particular, the only ion affected by the blockage of these channels is Cl , indicating that the disruption of this anion prevents NLRP3 activation (41)."