
IndraLab
Statements
reach
"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]."
reach
"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."
reach
"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."
reach
"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."
reach
"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)."