IndraLab

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N-acetyl-L-cysteine inhibits NLRP3. 9 / 9
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"The use of ROS scavenger N-acetylcysteine (NAC) partially reversed NLRP3 inflammasome activity in cells exposed to burn serum."
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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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"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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"In high glucose cultured cardiomyocytes, Klotho and N-acetylcysteine significantly downregulated intracellular reactive oxygen species generation and TXNIP and NLRP3 inflammasome activation."
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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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"Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE treated ECs."
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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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"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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"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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