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Amelioration of ethanol induced apoptotic DNA damage and ulcerative injuries in the mice gastric tissues by starch oral administration

pmid: 28849987
Nowadays, gastric ulcers have become very common gastrointestinal disorders and numerous natural plant extracts exert promising anti-ulcerative effects. Therefore, this study was designed to evaluate the possible protective effect of dietary starch against ethanol induced gastric ulcers in mice. Post-administration of dietary starch for three consecutive days caused remarkable ameliorations in hemorrhagic lesions in gastric mucus and significant suppression in % incidence of ulceration, ulcer index and ulcer score induced by ethanol single administration. Indeed, deep ulceration, necrosis, disruption and degeneration in large areas of mucosa layer together with dense inflammatory cells infiltration and edema in sub-mucosal layer induced by ethanol administration were attenuated by starch post-administration and normalized the tissue architecture of the stomach. This potential protective effect could be attributed to the potent anti-oxidative capacity of starch that causes scavenger of the reactive oxygen species and thereby decreasing single and double DNA stranded break inductions and apoptotic DNA damage revealed by returning the p53 and caspase-3 expression levels to the normal level compared to the ethanol treated group. In conclusion, dietary starch has a potent therapeutic effect against ethanol induced gastric ulcer in mice via its free radical scavengers ability. Thus, we recommended further studies on its possible use as antiulcer drugs.
Ethanol, Caspase 3, Administration, Oral, Central Nervous System Depressants, Apoptosis, Starch, Anti-Ulcer Agents, Mice, Oxidative Stress, Animals, Comet Assay, Stomach Ulcer, Tumor Suppressor Protein p53, Gastrointestinal Hemorrhage, DNA Damage
Ethanol, Caspase 3, Administration, Oral, Central Nervous System Depressants, Apoptosis, Starch, Anti-Ulcer Agents, Mice, Oxidative Stress, Animals, Comet Assay, Stomach Ulcer, Tumor Suppressor Protein p53, Gastrointestinal Hemorrhage, DNA Damage
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