Manuka Honey Exerts Antioxidant and Anti-Inflammatory Activities That Promote Healing of Acetic Acid-Induced Gastric Ulcer in Rats. (19th January 2017)

• Record Type: Journal Article
• Authors: Almasaudi, Saad B.; Abbas, Aymn T.; Al-Hindi, Rashad R.; El-Shitany, Nagla A.; Abdel-dayem, Umama A.; Ali, Soad S.; Saleh, Rasha M.; Al Jaouni, Soad K.; Kamal, Mohammad Amjad; Harakeh, Steve M.
• Other Names: Sforcin José Maurício Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2017(2017)
• Publication Date: 2017-01-19
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2017/5413917
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Gastric ulcers are a major problem worldwide with no effective treatment. The objective of this study was to evaluate the use of manuka honey in the treatment of acetic acid-induced chronic gastric ulcers in rats. Different groups of rats were treated with three different concentrations of honey. Stomachs were checked macroscopically for ulcerative lesions in the glandular mucosa and microscopically for histopathological alterations. Treatment with manuka honey significantly reduced the ulcer index and maintained the glycoprotein content. It also reduced the mucosal myeloperoxidase activity, lipid peroxidation (MDA), and the inflammatory cytokines (TNF- α, IL-1 β, and IL-6) as compared to untreated control group. In addition, honey-treated groups showed significant increase in enzymatic (GPx and SOD) and nonenzymatic (GSH) antioxidants besides levels of the anti-inflammatory cytokine IL-10. Flow cytometry studies showed that treatment of animals with manuka honey has normalized cell cycle distribution and significantly lowered apoptosis in gastric mucosa. In conclusion, the results indicated that manuka honey is effective in the treatment of chronic ulcer and preservation of mucosal glycoproteins. Its effects are due to its antioxidant and anti-inflammatory properties that resulted in a significant reduction of the gastric mucosal MDA, TNF- α, IL-1 β, and IL-6 and caused an elevation in IL-10 levels.