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N-acetyl-L-cysteine inhibits NLRP3. 13 / 13
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"Moreover, ROS was required for E. coli O157 : H7 induced NLRP3 assembly as inhibiting mitochondrial ROS release by ROS scavengers Mito-TEMPO and N-acetylcysteine abrogated NLRP3 inflammasome activation in Caco-2 cells in response to E. coli O157 : H7."
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"Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS)."
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"Mechanistic studies indicated that the addition of N-acetylcysteine (NAC), a ROS scavenger, inhibited NLRP3 activation and attenuated pyroptosis."
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"Additionally, these fibers displayed augmented activation of the NLRP3 inflammasome, accompanied by heightened ROS-dependent proximity between TXNIP and NLRP3, which was abolished by the antioxidant N-acetylcysteine (NAC)."
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"We reported previously that high glucose and lipopolysaccharide activate ROS-TXNIP-NLRP3 inflammasome signaling in GMCs, but ROS inhibitor N-acetylcysteine (NAC) could not completely inhibit the activation of NLRP3 inflammasome induced by high glucose, suggesting that there may be other pathways by which high glucose primes ROS-NLRP3 inflammasome signaling [XREF_BIBR]."
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"Additionally, N-acetylcysteine (NAC, 5 mM, a ROS scavenger) could inhibit the activation of NLRP3 inflammasome under SelW overexpression, indicating the SelW overexpression-induced NLRP3 inflammasome activation is a ROS-dependent manner (Fig. S2E)."
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"Budesonide and N-acetylcysteine inhibit activation of the NLRP3 inflammasome by regulating miR-381 to alleviate acute lung injury caused by the pyroptosis-mediated inflammatory response."
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"ROS scavenger N-acetyl-L-cysteine suppressed the activation of NLRP3 inflammasomes and alleviated atherosclerosis induced by HHcy60."
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"N-Acetyl-L-cysteine (NAC) administration also inhibited oxidative stress and activation of the calpain system and the NLRP3 inflammasome."
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"Application of the ROS scavenger N-acetylcysteine (NAC) can significantly inhibit the activation of NLRP3 and osteocytes pyroptosis."
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"In a mouse alveolar macrophage model induced by LPS and NETs, N-acetyl-L-cysteine (NAC) prevented NLRP3 inflammasomes from undergoing deubiquitination modification by binding to DUBs."
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"The ROS inhibitor , N-acetyl-l-cysteine ( NAC ) , significantly reduced IL-1beta production , and blocked NLRP3 and ASC upregulation after exposure to PrP106-126 in murine microglia ( Shi et al ., 2012 ) ."
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"In vitro , N-acetylcysteine ( NAC ) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression , in MOVAS cells treated with TNF-alpha ."
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