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Vanillin abrogates ethanol induced gastric injury in rats via modulation of gastric secretion, oxidative stress and inflammation.
- Source :
-
Toxicology reports [Toxicol Rep] 2015 Dec 12; Vol. 3, pp. 105-113. Date of Electronic Publication: 2015 Dec 12 (Print Publication: 2016). - Publication Year :
- 2015
-
Abstract
- Vanillin is commonly used as an additive in food, medicine and cosmetics, but its effect has not yet been studied in gastric injury. Therefore the effect of vanillin was studied in experimental gastric ulcer. Gastric secretion and acidity were studied in pylorus ligated rats. Ulcer index, levels of gastric mucus, malondialdehyde (MDA), myeloperoxidase activity (MPO), expression of nuclear factor kappa B (NF-κB) p65, and histopathological changes were determined in ethanol induced gastric ulcer. Pre treatment with vanillin significantly reduced gastric secretion ( P  < 0.001) and acidity ( P  < 0.0001) and gastric ulcer index scores ( P  < 0.001). and augmented the gastric mucosal defense. Vanillin significantly restored the depleted gastric wall mucus levels ( P  < 0.0001) induced by ethanol and also significantly attenuated ethanol induced inflammation and oxidative stress by the suppression of gastric MPO activity ( P  < 0.001), reducing the expression of NF-κB p65 and the increased MDA levels ( P  < 0.001). Vanillin was also effective in alleviating the damage to the histological architecture and the activation of mast cells induced by ethanol. Together the results of this study highlight the gastroprotective activity of vanillin in gastric ulcers of rats through multiple actions that include inhibition of gastric secretion and acidity, reduction of inflammation and oxidative stress, suppression of expression of NF-κB, and restoration of the histological architecture.
Details
- Language :
- English
- ISSN :
- 2214-7500
- Volume :
- 3
- Database :
- MEDLINE
- Journal :
- Toxicology reports
- Publication Type :
- Academic Journal
- Accession number :
- 28959528
- Full Text :
- https://doi.org/10.1016/j.toxrep.2015.11.001