Possible Interaction: Acetylcysteine and Dinoprostone

“Pretreatment with N-acetylcysteine NAC ) reduced COX-2 expression and PGE2 release induced by PDT.”

“ NAC (10 mM) inhibited accumulation of PGE2 and IL10 only; NBDI (10 μM) had no significant effect.”

“Whereas NAC suppressed production of CXCL8 by CSE-conditioned DCs, it augmented production of PGE2 and cellular COX-2 levels in maturing DCs.”

“ N‐acetylcysteine (NAC) significantly attenuated UVB‐induced PGE2 production, COX activity and COX‐2 mRNA expression indicating oxidative components might contribute to these events.”

“ N:-acetyl-L-cysteine and pyrrolidinedithiocarbamate, two inhibitors of reactive oxygen species (ROS), inhibit NNK-induced PGE2 synthesis by 41 and 44%, respectively.”

“The antioxidant N-acetylcysteine decreased UVB-induced EGF-R tyrosine phosphorylation and PGE2 synthesis to near-basal levels.”

“Furthermore, PGE2 production in the culture medium was increased in SB, whereas NAC decreased the PGE2 production.”

“The pre-treatment of LPS-stimulated PBMCs with NAC resulted in a significant decrease in PGE2 concentration in comparison to the cells treated with LPS alone (PGE2 level was 386.1±61.9pg/mL vs. 2078.9±157.9pg/mL, respectively, p<0.001).”

“Similar to the effect of RA, both NAC and NS-398 (COX-2 inhibitor) blocked CoCl2-induced COX-2 expression and PGE2 secretion.”

“Significantly, when combined with NAC, PGE2 extended the time window for a successful intervention, synergistically reducing apoptosis, improving liver enzymes, and preventing death.”