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Reversing gastric mucosal alterations during ethanol-induced chronic gastritis in rats by oral administration of Opuntia ficus-indica mucilage

机译:口服印度仙人掌黏液逆转乙醇诱发的慢性胃炎大鼠胃黏膜改变

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摘要

AIM: To study the effect of mucilage obtained from cladodes of Opuntia ficus-indica (Cactaceae) on the healing of ethanol-induced gastritis in rats.METHODS: Chronic gastric mucosa injury was treated with mucilage (5 mg/kg per day) after it was induced by ethanol. Lipid composition, activity of 5’-nucleotidase (a membrane-associated ectoenzyme) and cytosolic activities of lactate and alcohol dehydrogenases in the plasma membrane of gastric mucosa were determined. Histological studies of gastric samples from the experimental groups were included.RESULTS: Ethanol elicited the histological profile of gastritis characterized by loss of the surface epithelium and infiltration of polymorphonuclear leukocytes. Phosphatidylcholine (PC) decreased and cholesterol content increased in plasma membranes of the gastric mucosa. In addition, cytosolic activity increased while the activity of alcohol dehydrogenases decreased. The administration of mucilage promptly corrected these enzymatic changes. In fact, mucilage readily accelerated restoration of the ethanol-induced histological alterations and the disturbances in plasma membranes of gastric mucosa, showing a univocal anti-inflammatory effect. The activity of 5’-nucleotidase correlated with the changes in lipid composition and the fluidity of gastric mucosal plasma membranes.CONCLUSION: The beneficial action of mucilage seems correlated with stabilization of plasma membranes of damaged gastric mucosa. Molecular interactions between mucilage monosaccharides and membrane phospholipids, mainly PC and phosphatidylethanolamine (PE), may be the relevant features responsible for changing activities of membrane-attached proteins during the healing process after chronic gastric mucosal damage.
机译:目的:研究从仙人掌仙人掌的枝条获得的黏液对大鼠乙醇性胃炎的愈合作用。方法:慢性黏膜损伤(每天5 mg / kg)治疗由乙醇诱导。测定了胃黏膜质膜的脂质组成,5'-核苷酸酶(一种与膜相关的外切酶)的活性以及乳酸和乙醇脱氢酶的胞浆活性。结果:乙醇诱导胃炎的组织学特征为表面上皮丧失和多形核白细胞浸润。胃粘膜质膜中磷脂酰胆碱(PC)下降,胆固醇含量增加。此外,胞质活性增加,而醇脱氢酶的活性降低。粘液的施用迅速纠正了这些酶促变化。实际上,粘液很容易加速乙醇诱导的组织学改变和胃粘膜质膜紊乱的恢复,显示出明确的抗炎作用。结论5'-核苷酸酶的活性与胃黏膜质膜的脂质组成和流动性有关。结论:黏液的有益作用似乎与受损胃黏膜的质膜稳定有关。黏液单糖和膜磷脂之间的分子相互作用,主要是PC和磷脂酰乙醇胺(PE),可能是慢性胃粘膜损伤后愈合过程中改变膜连接蛋白活性的相关特征。

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