2000
DOI: 10.1080/096374800111113
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Effect of palm vitamin E on the healing of ethanol-induced gastric injury in rats

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Cited by 8 publications
(8 citation statements)
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“…The metabolism of EtOH generates superoxide radicals supporting lipid peroxidation which is known to be a mechanism of ethanol-induced gastric mucosal injury. Moreover, MDA is known to be a good indicator of the degree of lipid peroxidation [22][23][24][25]. In the current study, parallel to ulcer formation, a significant elevation in MDA content was observed once ethanol given orally and also indicate that SF pretreatment significantly prevents MDA production implying the idea that reduction in lipid peroxidation and cellular injury protecting the gastric tissue against ethanol-induced oxidative damage.…”
Section: Discussionsupporting
confidence: 61%
“…The metabolism of EtOH generates superoxide radicals supporting lipid peroxidation which is known to be a mechanism of ethanol-induced gastric mucosal injury. Moreover, MDA is known to be a good indicator of the degree of lipid peroxidation [22][23][24][25]. In the current study, parallel to ulcer formation, a significant elevation in MDA content was observed once ethanol given orally and also indicate that SF pretreatment significantly prevents MDA production implying the idea that reduction in lipid peroxidation and cellular injury protecting the gastric tissue against ethanol-induced oxidative damage.…”
Section: Discussionsupporting
confidence: 61%
“…PVE was also shown to be effective in increasing the PGE 2 level in rats given indomethacin [239] but not in ethanol-induced ulcers [246]. Prostaglandin is produced from arachidonic acid by the action of cyclooxygenase (COX) enzyme.…”
Section: Effects Of Tocotrienol On Peptic Ulcersmentioning
confidence: 99%
“…Another important protective factor in the gastric mucosa is the mucus covering it [251]. However, the gastric adherent mucus content was unaltered in rats fed with a diet containing various doses of TRF (60, 100, 150, and 300 mg/kg) for 4-8 weeks and administered absolute ethanol even though there was a reduction in gastric lesion index compared to the untreated control [240,242,244,246,249]. A similar finding was also observed in rats given a diet containing αTF (20, 30, 50, and 300 mg/kg) for 4-8 weeks and challenged with aspirin [240,242], which confirms that neither T3 or TF exerts any significant effect on gastric mucus production.…”
Section: Effects Of Tocotrienol On Peptic Ulcersmentioning
confidence: 99%
“…The mucus covers the mucosa of the gastrointestinal tract (Repetto & Llesuy, 2002). The gastric adherent mucus content was unaltered in rats that were fed a diet containing various doses of tocotrienol-rich fraction (60, 100, 150, and 300 mg/kg) for 4-8 weeks and administered absolute ethanol, indomethacin, or aspirin even though there was a reduction in gastric lesion index compared with the untreated control (Jaarin et al, 1999(Jaarin et al, , 2000(Jaarin et al, , 2002Nafeeza et al, 2002;Qodriyah et al, 2002). A similar finding was also observed in rats given a diet containing a-tocopherol (20, 30, 50, and 300 mg/kg) for 4-8 weeks and challenged with aspirin (Jaarin et al, 2002;Nafeeza et al, 2002).…”
Section: Diminished Endogenous Gastroprotective Factorsmentioning
confidence: 99%
“…On one hand, a-tocopherol increased gastric PGE 2 level in many gastric lesion models (Fesharaki et al, 2006, Jiang et al, 2009Tariq, 1988). Tocotrienol, on the other hand, was also not effective in increasing the PGE 2 level in rats given indomethacin (Qodriyah et al, 2002) or ethanol (Jaarin et al, 2000). However, when the two were combined, a protective effect of the combination was observed (Nafeeza & Kang, 2005).…”
Section: Diminished Endogenous Gastroprotective Factorsmentioning
confidence: 99%