IndraLab
Statements
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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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"A previous study has suggested that Ac-YVAD-CMK, BAY11-7082, or NAC attenuate HG- and H/R-stimulated H9C2 cell injury and suppress NLRP3 inflammasome-dependent pyroptosis.170 Suppression of the NLRP3 inflammasome and ROS synthesis attenuates cell injury and pyroptosis in LPS-stimulated H9C2 cells under HG and H/R conditions.170 BAY11-7082 and NAC treatment can hinder NLRP3 inflammasome by decreasing the NLRP3, ASC, and NF-κB p65 protein expression levels in LPS and HG+H/R-stimulated H9C2 cells."
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"In addition, functional experiments confirmed that both ROS scavenger NAC and METTL3-ablation downregulated NLRP3, GSDMD-C, cleaved Caspase-1 and ASC to restrain pyroptotic cell death and decreased the expression levels of IL-1β, IL-18, IL-6 and TNF-α to restrain inflammatory cytokines expression in Mtb-infected macrophages."
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"NAC significantly abrogated PrP106-126-induced NALP3 and ASC upregulation; the mRNA levels of NALP3 and ASC significantly decreased after NAC treatment in PrP106-126-treated microglia and dropped to 68% and 54%, respectively, of the levels seen in microglia treated with PrP106-126 only."
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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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"Bengalli et al. found that PM10 induced ROS activated NLRP3 inflammasome and consequently promoted thematuration of pro-IL-1b into bioactive IL-1b, and they also discovered that NAC significantly inhibited this PM10mediated activation of NLRP3 inflammasome and blocked IL-1b production (Bengalli et al., 2013)."
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"In the present study, we found that the ROS inhibitor NAC significantly reduced the production of IL-1beta, and blocked NALP3 and ASC upregulation after exposure to PrP106-126, suggesting a role of ROS generation in the activation of the inflammasome in PrP106-126-stimulated microglia."
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"Previous research, however, has revealed that while N-acetyl cysteine (NAC) suppresses NLRP3 activation by blocking ROS in wild-type macrophages stimulated with lipopolysaccharide (LPS)/silica or LPS/nigericin, caspase-1 activation is not inhibited when NLRP3 expression is uncoupled from the priming signal by stable overexpression."
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"Furthermore, the mechanism study found that PPVI could activate the NF-kappaB signaling pathway via increasing reactive oxygen species (ROS) levels in A549 and H1299 cells, and N -acetyl-L-cysteine (NAC), a scavenger of ROS, remarkably inhibited the cell death, and the activation of NF-kappaB and the NLRP3 inflammasome in PPVI treated A549 and H1299 cells."