Hend El Sayed Nasr El sayed
Asst. Professor
The ameliorative impacts of wheat germ oil against ethanol-induced gastric ulcers: involvement of anti-inf lammatory, antiapoptotic, and antioxidant activities
• 2022
Publication Information
Authors
Rabab Shaban El-shafey1, Samar H. Baloza2, Lina Abdelhady Mohammed3, Hend Elsayed Nasr3, Mohamed Mohamed Soliman4,
*,
Heba I. Ghamry5, Salwa A. Elgendy6
Keywords
Not Available
Journal
Not Available
Publisher
Not Available
Volume
Not Available
Issue
Not Available
Pages
Not Available
publication.type
Local
Paper Link
Not Available
Supplementary Materials
Not Available
Abstract
This study examined if wheat germ oil (WGO) has gastroprotective impacts against ethanol-induced gastric ulcer in rats. Rats were
assigned into control, WGO, ethanol, omeprazole + ethanol, and WGO + ethanol. WGO prevented gastric ulceration and damage
induced by ethanol, the same effect induced by omeprazole, a widely known medication used for gastric ulcer treatment.WGO reduced
gastric ulcer index, nitric oxide, and malondialdehyde levels in the stomach. WGO boosted the expression of nuclear factor erythroid
2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Bcl2, and the antioxidants. WGO showed inf lammatory and anti-inf lammatory
impacts through the control of interleukin (IL)-1β, Tumor necrosis factor alpha (TNF-α), and IL-10 that were altered in ethanoladministered rats. Ethanol up-regulated caspase-3 and nuclear factor-kappa B (NF-kB) expression and showed histopathological
changes such as necrosis and mucosal degeneration that were mitigated by pre-administration of WGO. Moreover, WGO decreased
gastric immunoreactivity of NF-kB and increased transforming growth factor beta-1 (TGF-β1) that were associated with upregulation
of Nrf2, heme oxygenase-1 (HO-1), and antioxidant expression and production. In conclusion,WGO reduced ethanol-induced stomach
toxicity by regulating genes involved in oxidative stress, inf lammation, and apoptotic/antiapoptotic pathways.
assigned into control, WGO, ethanol, omeprazole + ethanol, and WGO + ethanol. WGO prevented gastric ulceration and damage
induced by ethanol, the same effect induced by omeprazole, a widely known medication used for gastric ulcer treatment.WGO reduced
gastric ulcer index, nitric oxide, and malondialdehyde levels in the stomach. WGO boosted the expression of nuclear factor erythroid
2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Bcl2, and the antioxidants. WGO showed inf lammatory and anti-inf lammatory
impacts through the control of interleukin (IL)-1β, Tumor necrosis factor alpha (TNF-α), and IL-10 that were altered in ethanoladministered rats. Ethanol up-regulated caspase-3 and nuclear factor-kappa B (NF-kB) expression and showed histopathological
changes such as necrosis and mucosal degeneration that were mitigated by pre-administration of WGO. Moreover, WGO decreased
gastric immunoreactivity of NF-kB and increased transforming growth factor beta-1 (TGF-β1) that were associated with upregulation
of Nrf2, heme oxygenase-1 (HO-1), and antioxidant expression and production. In conclusion,WGO reduced ethanol-induced stomach
toxicity by regulating genes involved in oxidative stress, inf lammation, and apoptotic/antiapoptotic pathways.