Filep J, Hermán F, Braquet P
Department of Pathophysiology, Semmelweis University Medical School, Budapest, Hungary.
Lipids. 1991 Dec;26(12):1356-8. doi: 10.1007/BF02536566.
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.
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。