Comparative effect of palm vitamin E and ranitidine on the healing of ethanol-induced gastric lesions in rats

Abstract

The effect of palm vitamin E on the healing of ethanol-induced gastric lesion was compared with ranitidine. Fifty-six male rats of Sprague-Dawley species (200-250 g of weight) were randomly divided into three groups (N = 14). Gastric mucosal injury was induced by orogastric tube administration of 0.5 ml 100% ethanol. Immediately after induction, Group I (k) rats was fed with a normal diet (control), group II (p) was fed palm vitamin E enriched diet (150 mg/kg food), Group III(r) was treated with ranitidine 30 mg/kg body weight intraperitoneally and Group IV (p + r) was fed with palm vitamin E and treated with ranitidine 30 mg/kg body weight intraperitoneally of the same dose. The rats were killed at the end of 1 week and 3 weeks of treatment or feeding. The rate of gastric healing was faster in palm vitamin E treated group compared to control and ranitidine treated groups as shown by a lower mean ulcer index. The effect was seen as early as the first week of treatment whereas ranitidine did not show any healing effect even after 3 weeks of therapy. Neither gastric acidity nor gastric mucus production are involved in gastroprotective effect of palm vitamin E. The most probable mechanism is via reducing lipid peroxidation process as shown by a significant decrease in gastric MDA.

The ameliorative effect of dates (Phoenix dactylifera L.) on ethanol-induced gastric ulcer in rats

“…It has been reported that treatment with melatonin prevents gastric ulcerogenesis and decreases ulcer index (Bandyopadhyan et al, 2001;Bubenik, 2002). Vitamin E in palm oil has also been shown to reduce ethanol-induced gastric ulcer (Jarrin et al, 1999). Taken together, these results corroborate our present finding of an ameliorative action of dates on ethanol-induced gastric ulceration, possibly due to its relatively high content of antioxidant substances.…”

Potential Role of Tocotrienols on Non-Communicable Diseases: A Review of Current Evidence

“…Gastric ulcers induced by ethanol exposure in rats were significantly reduced with the supplementation of PVE at 150 mg/kg in food for 3 weeks [249,250]. The ulcers healing was also accelerated when PVE (150 mg/kg food) was given post-ulcer induction with ethanol [249]. These effects were achieved by retarding the lipid peroxidation induced by ethanol.…”

“…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.…”

Vitamin E: A potential therapy for gastric mucosal injury

“…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).…”