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镁对吲哚美辛诱导的大鼠胃溃疡的抗溃疡作用机制

Anti-ulcerogenic mechanism of magnesium in indomethacin induced gastric ulcer in rats.

作者信息

Adewoye E O, Salami A T

机构信息

Department of Physiology, College of Medicine, University of Ibadan, Ibadan.

出版信息

Niger J Physiol Sci. 2013 Dec 20;28(2):193-9.

PMID:24937396
Abstract

The gastric mucosa is continuously exposed to various agents like food condiments, spices, alcohol, acids and drugs, some of which are implicated in the pathogenesis of gastric ulcer. Magnesium compounds commonly used as laxatives and antacids have been reported to prevent ulcer formation but the mechanisms underlying this potential is unknown. This study therefore seeks to evaluate the gastro-protective mechanism of magnesium in the stomach through its effect on the parietal and mucus cells. Thirty-six male albino rats divided into 6 groups of 6 rats each were used. Group 1 was control, Group 2 was ulcer induced and untreated, Group 3 was treated with 500mg/kg b.w magnesium alone, Group 4 was pre-treated with 500mg/kg b.w magnesium before inducing ulcer, Group 5 was pre-treated with 500mg/kg b.w magnesium and 20mg/kg omeprazole 4 hours before inducing ulcer, Group 6 was treated with 20mg/kg omeprazole 4 hours before inducing ulcer. Animals were sacrificed 6 hours after ulcer induction and their stomachs were removed for ulcer scoring and histological analysis. A significant reduction was observed in the ulcer scoring of magnesium pre-treated ulcerated rats (9.4±0.8) compared with ulcerated untreated (20.8±0.9) groups. Parietal cell count of magnesium pre treated ulcerated group significantly decreased (169.7±18.9) compared with ulcerated untreated group (310.5±34.7). Mucous cell count of magnesium pre-treated ulcerated group (264.6±8.3) significantly increased compared with ulcerated untreated group (170.0±17.7). This study shows that magnesium possesses anti-ulcerogenic properties due to its ability to reduce the number of parietal cell and increase mucous cell counts.

摘要

胃黏膜持续暴露于各种物质,如食物调味料、香料、酒精、酸和药物,其中一些与胃溃疡的发病机制有关。常用作泻药和抗酸剂的镁化合物已被报道可预防溃疡形成,但其潜在机制尚不清楚。因此,本研究旨在通过镁对壁细胞和黏液细胞的作用来评估其在胃中的胃保护机制。使用36只雄性白化大鼠,将其分为6组,每组6只。第1组为对照组,第2组诱导溃疡但未治疗,第3组仅用500mg/kg体重的镁治疗,第4组在诱导溃疡前用500mg/kg体重的镁预处理,第5组在诱导溃疡前4小时用500mg/kg体重的镁和20mg/kg奥美拉唑预处理,第6组在诱导溃疡前4小时用20mg/kg奥美拉唑治疗。溃疡诱导6小时后处死动物,取出胃进行溃疡评分和组织学分析。与未治疗的溃疡组(20.8±0.9)相比,镁预处理的溃疡大鼠的溃疡评分显著降低(9.4±0.8)。与未治疗的溃疡组(310.5±34.7)相比,镁预处理的溃疡组的壁细胞计数显著降低(169.7±18.9)。与未治疗的溃疡组(170.0±17.7)相比,镁预处理的溃疡组的黏液细胞计数(264.6±8.3)显著增加。本研究表明,镁具有抗溃疡特性,因为它能够减少壁细胞数量并增加黏液细胞计数。

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