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磷酸铝对大鼠乙醇诱导的胃损伤的预防作用:内源性前列腺素和巯基的作用

Prevention by aluminium phosphate of gastric lesions induced by ethanol in the rat: role of endogenous prostaglandins and sulfhydryls.

作者信息

Duchateau A, Thiefin G, Varin-Bischoff S, Garbe E, Zeitoun P

机构信息

Laboratory of Cellular Digestive Morphology, University of Medicine, Reims, France.

出版信息

Histol Histopathol. 1990 Jan;5(1):89-94.

PMID:2134361
Abstract

This study was designed to demonstrate the cytoprotective effect of an antacid containing aluminium phosphate (Phosphalugel) against ethanol-induced gastric injury in the rat and to determine whether this cytoprotective effect is mediated by endogenous prostaglandins and sulfhydryls. We have quantitatively evaluated gastric mucosal lesions using macroscopic and histological techniques one hour after ethanol administration. Two ml of aluminium phosphate given orally one hour before administration of 2 ml of 100% ethanol significantly (p less than 0.01) reduced the area of macroscopic lesions induced by ethanol (3.3 +/- 0.9%) when compared to distilled water (20 +/- 4.8%). The histological study showed that aluminium phosphate prevented deep tissue necrosis. However, it did not protect surface epithelial cells against ethanol injury. Pretreatment with indomethacin, 5 mg/kg sc one hour before aluminium phosphate, slightly but significantly (p less than 0.05) reduced the cytoprotective effect of aluminium phosphate. Macroscopic lesions occupied 4.3 +/- 0.94% and 1.88 +/- 0.41% of total mucosal area in indomethacin group and in vehicle group, respectively. On the other hand, the sulfhydryl blocker, N-ethyl-maleimide, 10 mg/kg sc, given one hour before aluminium phosphate, completely abolished the cytoprotective effect of aluminium phosphate (32.92 +/- 4.85% in N-ethyl-maleimide group versus 3.78 +/- 1.41% in vehicle group; p less than 0.01). These results show that aluminium phosphate has a cytoprotective effect against ethanol injury in the rat. This property appears to be mediated by both endogenous prostaglandins and sulfhydryls.

摘要

本研究旨在证明含磷酸铝(磷酸铝凝胶)的抗酸剂对大鼠乙醇诱导的胃损伤的细胞保护作用,并确定这种细胞保护作用是否由内源性前列腺素和巯基介导。我们在给予乙醇1小时后,使用宏观和组织学技术对胃黏膜损伤进行了定量评估。在给予2 ml 100%乙醇前1小时口服2 ml磷酸铝,与蒸馏水组(20±4.8%)相比,显著(p<0.01)降低了乙醇诱导的宏观损伤面积(3.3±0.9%)。组织学研究表明,磷酸铝可防止深层组织坏死。然而,它并不能保护表面上皮细胞免受乙醇损伤。在给予磷酸铝前1小时皮下注射5 mg/kg消炎痛预处理,略微但显著(p<0.05)降低了磷酸铝的细胞保护作用。消炎痛组和溶剂组的宏观损伤分别占总黏膜面积的4.3±0.94%和1.88±0.41%。另一方面,在给予磷酸铝前1小时皮下注射10 mg/kg巯基阻断剂N-乙基马来酰胺,完全消除了磷酸铝的细胞保护作用(N-乙基马来酰胺组为32.92±4.85%,溶剂组为3.78±1.41%;p<0.01)。这些结果表明,磷酸铝对大鼠乙醇损伤具有细胞保护作用。这种特性似乎由内源性前列腺素和巯基共同介导。

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