Quercetin Oxidation Metabolite Present in Onion Peel Protects Caco-2 Cells against the Oxidative Stress, NF-κB Activation, and Loss of Epithelial Barrier Function Induced by NSAIDs

The potential of 2-(3,4-dihydroxybenzoyl)-2,4,6-trihydroxy-3(2H)-benzofuranone (BZF), a quercetin oxidation metabolite, and that of a BZF-rich onion peel aqueous extract (OAE) to protect Caco-2 monolayers against the oxidative stress (OS) and an increased permeability (IP) induced by five nonsteroidal anti-inflammatory drugs (NSAIDs) (indomethacin, didofenac, piroxicam, ibuprofen, and metamizole) were investigated. Under identical OS conditions, the NSAIDs substantially differed in their ability to induce an IP and/or NF-kappa B activation. The OAE (100 nM BZF) protected in identical magnitude (84-86%) against OS but in a highly dissimilar manner against the IP (18-73%). While all NSAIDs activated NF-kappa B, the OAE prevented only that induced by indomethacin. Results reveal that the IP has no direct relationship with the OS and that with the exception of indomethacin, the prevention of NSAIDs-induced OS and/or NF-kappa B activation plays no fundamental role in the IP-protecting effect of OAE. These results warrant the in vivo evaluation of OAE against indomethacin-induced loss of intestinal barrier function.

Automated summary

The study investigated the protective effects of BZF and BZF-rich OAE against oxidative stress and increased permeability induced by NSAIDs, finding that the prevention of NSAIDs-induced oxidative stress and NF-kappa B activation plays no fundamental role in the IP-protecting effect of OAE, except for with indomethacin.