ubiquinone and Stomach-Ulcer

Piroxicam (PM) is an oxicam-NSAID commonly recommended for various pain and associated inflammatory disorders. However, it is reported to have a gastric and hepato-renal toxic effect. Therefore, the current research was planned to investigate the possible mechanisms behind the mitigating action of the coenzyme (CoQ10), a natural, free radical scavenger, against PM tissue injury. Rats were assigned to five equal groups; Control, CoQ10 (10 mg/kg, orally), PM (7 mg/kg, i.p.), CoQ + PM L, and CoQ + PM H group. After 28 days, PM provoked severe gastric ulceration and marked liver and kidney damage indicated by an elevated gastric ulcer index and considerable alteration in liver and kidney biochemical tests. The toxic effects might be attributed to mitochondrial dysfunction and excess generation of reactive oxygen species (ROS), as indicated by enhanced malondialdehyde (MDA) levels along with decreased reduced-glutathione (GSH) levels and catalase (CAT) activity. Apoptotic cell death also was demonstrated by increased regulation of activated caspase-3 in the stomach, liver, and kidney tissues. Interestingly, external supplementation of CoQ10 attenuated the PM-inflicted deleterious oxidative harm and apoptosis. This ameliorative action was ascribed to the free radical scavenging activity of CoQ10.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Caspase 3; COVID-19; Dietary Supplements; Free Radical Scavengers; Kidney; Liver; Male; Malondialdehyde; Oxidation-Reduction; Oxidative Stress; Piroxicam; Rats; Rats, Wistar; Reactive Oxygen Species; Stomach; Stomach Ulcer; Ubiquinone

Alcohol consumption is frequently associated with gastric mucosal lesions. The purpose of this study was to determine the effect of Coenzyme-Q10 (CoQ10) supplementation on the ethanol-induced gastric mucosal damage in a rat model.. Sixty-four female wistar albino rats were randomly divided into 8 groups (n = 8). Studies were performed in ethanol induced gastric ulcer model in Wistar albino rats. Famotidine at a dose of 5 mg/kg or 20 mg/kg and CoQ10 at a single dose of 10 mg/kg or 20 mg/kg and 30 mg/kg for 7 days were administered as pretreatment. All the rats in study groups received 2 ml/kg ethanol 95 % intragastrically, 30 minutes after pretreatment. Four hour after ethanol administration, all rats were sacrificed and their stomachs were removed under ketamin anaesthesia. Gastric protection was evaluated by measuring the ulcer index, MDA concentrations, and histopathological studies.. Rats pretreated either with famotidine or CoQ10 had significantly diminished gastric mucosal damage which was assessed with gross and microscopic analysis (p < 0.00625). MDA levels were significantly lower in famotidine 20 mg/kg and CoQ10 pretreatment for 7 days group (p < 0.00625).

Topics: Animals; Anti-Ulcer Agents; Dose-Response Relationship, Drug; Ethanol; Female; Gastric Mucosa; Plant Extracts; Random Allocation; Rats; Rats, Wistar; Stomach Ulcer; Ubiquinone; Vitamins

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 E₂ 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 E₂ 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 E₂ levels that were increased above normal by sucralfate. CoQ10-mediated gastroprotective effect involves preservation of microvascular permeability, elevation of prostaglandin E₂, improvement of redox status, as well as boosting of nitric oxide. Nevertheless, maintaining gastric mucus content is ruled out.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Capillary Permeability; Dietary Supplements; Dinoprostone; Gastric Mucosa; Glutathione; Glutathione Peroxidase; Indomethacin; Lipid Peroxides; Male; Mucus; Nitric Oxide; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Wistar; Stomach Ulcer; Ubiquinone

As one of the factors contributing to the intractability of chronic gastric ulcer, the effect of hypoxia is examined in this paper, based upon the experimental acetic acid ulcer in the stomach of Wistar rats. Results indicate that hypoxia has a harmful influence on the healing process of chronic, gastric ulcer in rats, and also that this effect of hypoxia can be prevented by administration of Coenzyme Q10 in diet.

Topics: Acetates; Animals; Gastric Mucosa; Hypoxia; Male; Pylorus; Rats; Stomach Ulcer; Time Factors; Ubiquinone