European Journal of Biomedical and Pharmaceutical Sciences

THE POTENTIAL PROTECTIVE EFFECTS OF ELLAGIC ACID AND COENZYME Q10 AGAINST EXPERIMENTALLY-INDUCED GASTRIC ULCER IN RATS

Sabri N. Hamed*, Samia S. Sokkar and Sally E. Abu-Risha

ABSTRACT

Gastric ulcer is a persistent gastrointestinal disease; it involves 10% of the world’s population and can lead to bleeding and death. The presented study was conducted to spotlight the leverage of Ellagic (EA) acid and Coenzyme Q10 (CoQ10) as gastro-protective agents against gastric ulcers in rat models, and we aimed to focus on gaining a better understanding of the effects and the mechanistic pathways of action of EA and CoQ10. Male rats were distributed to seven groups: group I normal vehicle normal control, group II indomethacin (INDO) ulcer control, and pre-treatment groups that include; group III ranitidine (RA), group IV EA, group V EA + RA, group VI CoQ10, and group VII CoQ10 + RA. For 10 days before induction of the ulcer with INDO, each rat received either vehicle (carboxymethyl cellulose +1% tween 80) or other doses intragastrically, and on day 10, they received INDO. After 6 hours of INDO treatment, rats were sacrificed, and their stomachs were excised to evaluate histopathological changes, gastric acidity, inflammatory molecules, oxidative stress, and apoptotic mediators. Results showed that a single 100mg/kg dose of INDO significantly elevated gastric acidity, expression of caspase-3, malondialdehyde (MDA), and gastric tumor necrosis factor-alpha (TNF-), and significantly diminished levels of reduced glutathione (GSH), nitric oxide (NO), and superoxide dismutase (SOD) activity compared to normal control. Pre-treatment with EA and CoQ10, each alone and in combination with RA, preserved the histopathological changes and gastric acidity within the normal limits and produced significant raises in GSH, SOD, NO levels, and significant decline in MDA, TNF-α gastric levels, as well as a decrease in caspase-3 up-regulation, compared to ulcer control values.

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