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血小板活化因子可能介导大鼠地塞米松诱导的胃损伤。

Platelet-activating factor may mediate dexamethasone-induced gastric damage in the rat.

作者信息

Filep J, Hermán F, Braquet P

机构信息

Department of Pathophysiology, Semmelweis University Medical School, Budapest, Hungary.

出版信息

Lipids. 1991 Dec;26(12):1356-8. doi: 10.1007/BF02536566.

DOI:10.1007/BF02536566
PMID:1819733
Abstract

The possible role of platelet-activating factor (PAF) in dexamethasone-induced gastric mucosal damage was studied in rats. PAF was measured by a platelet aggregation assay. The identity of the PAF-like product recovered from gastric tissues was ascertained by thin-layer chromatography and high-pressure liquid chromatography. Low levels of PAF were detected in the normal rat stomach, while in dexamethasone-treated animals PAF levels were significantly higher. Pretreatment of the animals with BN 52021, a specific PAF receptor antagonist, significantly attenuated dexamethasone-induced mucosal injury. These findings suggest that PAF may be a mediator of mucosal damage induced by glucocorticoids.

摘要

在大鼠中研究了血小板活化因子(PAF)在 dexamethasone 诱导的胃黏膜损伤中的可能作用。通过血小板聚集试验测量 PAF。从胃组织中回收的 PAF 样产物的特性通过薄层色谱法和高压液相色谱法确定。在正常大鼠胃中检测到低水平的 PAF,而在接受 dexamethasone 治疗的动物中,PAF 水平显著更高。用特异性 PAF 受体拮抗剂 BN 52021 对动物进行预处理,可显著减轻 dexamethasone 诱导的黏膜损伤。这些发现表明,PAF 可能是糖皮质激素诱导的黏膜损伤的介质。

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1
Platelet-activating factor may mediate dexamethasone-induced gastric damage in the rat.血小板活化因子可能介导大鼠地塞米松诱导的胃损伤。
Lipids. 1991 Dec;26(12):1356-8. doi: 10.1007/BF02536566.
2
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Microvascular actions of platelet-activating factor on rat gastric mucosa and submucosa.血小板活化因子对大鼠胃黏膜和黏膜下层的微血管作用。
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Platelet-activating factor in normal rat uterus.正常大鼠子宫中的血小板活化因子
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Picomole doses of platelet-activating factor predispose the gastric mucosa to damage by topical irritants.皮摩尔剂量的血小板活化因子会使胃黏膜更易受到局部刺激物的损伤。
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Gastrointestinal plasma leakage in endotoxic shock. Inhibition by prostaglandin E2 and by a platelet-activating factor antagonist.内毒素休克时的胃肠道血浆渗漏。前列腺素E2和血小板活化因子拮抗剂的抑制作用。
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