Effects of Vitamin B on experimentally induced gastric ulcers in rodents
Keywords:Vitamin deficiency, gastro-protection, Helicobacter pylori, nutrition
Background: Peptic ulcer disease (PUD) is associated with water soluble vitamin deficiencies. B group vitamins play vital roles in maintenance of essential body functions. PU patients are found to present with Vitamin B deficiency and high rates of Helicobacter pyloric infection. This study aims to investigate the effect of vitamin B (VB) on experimentally induced gastric ulcers in mice
Method: Gastric ulcers were induced in adult Swiss albino mice using absolute ethanol, a nonsteroidal anti-inflammatory agent, diclofenac and acetic acid. Animal were treated for 7 days with vitamin B at 12.5, 25 and 50 mg/kg before ulcer induction with ethanol and diclofenac, while in the acetic acid induced ulcers, treatment (VB 50 mg/kg) was administered for 14 and 28 days post ulcer induction. The degree of gastric ulceration was scored after which tissues subjected to histological analysis
Results: The results showed that vitamin B ameliorated ulceration caused by absolute ethanol, diclofenac and acetic acid. In the ethanol induce ulcer, pretreatment with VB produced dosedependent reduction in severity of ulcer when compared to control group. Ulceration of gastric mucosa was inhibited by 3.57%, 23.86% and 55.71% at 12.5, 25 and 50 mg/kg of VB respectively. Omeprazole produced an inhibition of 69.71% at 20mg/kg. VB similarly inhibited diclofenac induced ulceration by 54.31%, 69.05% and 78.94% respectively at tested doses, while omeprazole had 87.79%. For the acetic acid-induced ulcer animals, treatment significantly increased pH of gastric contents when compared with control. Histological analysis revealed dose-dependent (ethanol and diclofenac) and time - dependent (Acetic acid) decrease in severity of damage caused by the ulcerogens on treatment with VB
Conclusion: These findings suggest that vitamin B possesses potential gastro-protective effects.
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