Coenzyme Q10 A novel gastroprotective effect via modulation of vascular permeability, prostaglandin E2, nitric oxide and redox status in indomethacin-induced gastric ulcer model

Coenzyme Q10 is an essential cofactor in the mitochondrial electron transport pathway and is endowed for its potent antioxidant capacity characters that endorse its implication in several clinical practices and as a food supplement Nevertheless its potential gastro-protective effect, in acute models has never been assessed which is the objective of this study Since indomethacin mediated gastropathy is multifaceted including mitochondrial dysfunction and generation of reactive oxygen species thus the indomethacin induced gastric injury serves as a convenient animal model for this work. Rats treated with indomethacin revealed mucosal hemorrhagic lesions increased microvascular permeability and inhibited prostaglandin E-2 and mucus content Redox imbalance was reflected by decreased mucosal glutathione (GSH) nitric oxide and glutathione peroxidase contents/activity along with elevated lipid peroxides Pretreatment with CoQ10 caused discernible decrease in indomethacin-induced gastric lesions vascular permeability and lipid peroxide content In addition prostaglandin E-2 and GSH levels were restored while those of nitric oxide and glutathione peroxidase were elevated significantly above normal however mucus formation was not altered significantly The positive effects were comparable to those of sucralfate the standard drug used herein except for the mucus and prostaglandin E-2 levels that were increased above normal by sucralfate CoQ10-mediated gastroprotective effect Involves preservation of microvascular permeability elevation of prostaglandin E-2 improvement of redox status as well as boosting of nitric oxide Nevertheless maintaining gastric mucus content is ruled out (C) 2010 Elsevier B V All rights reserved