Possible Interaction: Acetylcysteine and Bismuth Subsalicylate

“Suppressing either oxidative stress or ER stress was protective against light damage in 661W and ARPE-19 cells and N-acetyl-L-cysteine treatment markedly inhibited the activation of ER stress caused by light exposure.”

“In addition, inhibition of reactive oxygen species using N-acetylcysteine attenuated ER stress , expression of osteoclast-specific marker genes, and RANKL-induced CREBH activation.”

“ N-acetylcysteine , a ROS scavenger, diminished ER stress and autophagy induction effects.”

“ ER stress and apoptosis caused by TDZ were prevented by ROS inhibitor N-acetyl-L-cysteine ( NAC ) and protein synthesis inhibitor cycloheximide.”

“Furthermore, blocking ROS with NAC inhibited SW-induced ER stress , as evidenced by the downregulation of GRP78, phosphorylated (p)-protein kinase R-like ER kinase (PERK), p-inositol-requiring kinase 1α (IRE1α), p-50 activating transcription factor 6α and CHOP.”

“Consistently, our data revealed as well that mitigation of intracellular ROS levels with antioxidant NAC markedly attenuated H2O2-induced AMPK activation and ER stress.”

“ N-acetylcysteine and 4-phenylbutyric acid inhibited NPPB-induced oxidative stress, ER stress and apoptosis.”

“Meanwhile, the activation of the NF-E2-related factor-2 (NRF2)-driven stress gene activation, a key element involved in HIC, was suppressed by NAC.”

“Pre-treatment with NAC , a ROS production inhibitor, significantly reduced ER stress and apoptosis-related proteins induced by PD.”

“Furthermore, costunolide induced ROS generation, while the antioxidant N‐acetyl cysteine (NAC) effectively blocked ER stress and apoptosis activation, suggesting that ROS acts as an upstream signaling molecule in triggering ER stress and mitochondrial apoptotic pathways.”