recursor inside cells. The latter metabolite naturally occurs in precise tissues of onions and shallots but not in many of the quercetin-rich plant foods studied to date. In vitro studies conducted with Q-BZF as a pure compound and as a part of an aqueous extract obtained from the outer scales of onions HIV-1 Species revealed the capacity of Q-BZF to defend Caco-2 cells against oxidative anxiety, mitochondrial and lytic damage induced by ROS for example hydrogen peroxide or NSAIDs. The usage of NSAIDs as ROS-generating agents has opened the possibility of projecting the potential use of Q-BZF (and OAE) for defending against a few of the far more serious adverse gastrointestinal effects linked with all the use of NSAIDs. Inside such a conceptual frame of particular interest, there has been the demonstration that nanomolar concentrations of Q-BZF (or Q-BZF contained in OAE) safeguard Caco-2 monolayers against the oxidative pressure plus the enhance in paracellular permeability induced by NSAIDs. Towards exactly the same aim, studies performed in rats have lately demonstrated that the loss of epithelial barrier function induced by indomethacin is completely abolished by the oral administration of exceptionally low doses of Q-BZF contained in OAE. Although the exact mechanisms underlying the intestinal barrier function-protecting impact of Q-BZF remains to be elucidated, the above in vivo studies revealed that such protection may be mechanistically related using the in vivo capability with the Q-BZF-containing extract to COX-2 Compound upregulate the activity of certain antioxidant enzymes by way of the Nrf2 pathway and to abolish the indomethacin-induced activation of NF-B. This dual capacity of Q-BZF warrants additional evaluation under diverse conditions in which controlling the oxidative pressure and/or preventing the activation of NF-B appear to become critical for the prevention of certain pathologies.Author Contributions: H.S. conceived the topic. H.S. and J.F. drafted the manuscript. F.S. in addition to a.C.d.C. offered vital feedback. H.S. and J.F. revised the manuscript. All authors have study and agreed for the published version in the manuscript. Funding: This operate was supported by the projects FONDECYT-1190053 and FONDEF-VIU20P0005. Conflicts of Interest: The authors declare no conflict of interest.AbbreviationsARE antioxidant response elements BZF 2-(benzoyl)-2-hydroxy-3(2H)-benzofuranone derivative(s) Caco-2 human colonic adenocarcinoma CAT catalase two of 30 CYP cytochrome P450 DPPH 2,2-diphenyl-1-picrylhydrazyl EpRE electrophile response components ing endogenous ROS-scavenging/reducingdextran reFITC molecules (e.g., 3-kDa dextran conjugated with fluorescein isothiocyanate gamma glutamate-cysteine ligase, -Glu ys ligase -Glu ys ligase), gamma glutamate ysteine ligase or needed by some ROS-reducing enzymes (e.g., decreased GI gastrointestinal GSH reduced glutathione athione reductase, GSSGred). GSHpx defense mechaglutathione peroxidase ooperative array of enzyme-based antioxidant GSSGred umber of non-enzymatically acting antioxidant molecules,glutathione reductase of HO-1 heme ne (GSH), ubiquinol, dehydrolipoic acid, melatonin, ferritin, oxygenase-1 Keap1 Kelch-like ECH-associated protein 1 llothioneins are endogenously synthesized [8], when -tocophNF-B nuclear aspect kappa B noids and phenolics are acquired by way of dietary sources [9]. NQO1 NAD(P)H:quinone oxidoreductase 1 es, academia and business have paid an incredible deal of consideration to Nrf2-Keap1 nuclear element (erythroid-derived two)-like 2 vonoids, due
