PAF-mediated pulmonary edema:: a new role for acid sphingomyelinase and ceramide
PAF-mediated pulmonary edema:: a new role for acid sphingomyelinase and ceramide
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DOI：
10.1038/nm977
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发表时间：
2004-02-01
期刊：
影响因子：
82.9
通讯作者：
Uhlig, S
中科院分区：
文献类型：
--
作者：
Göggel, R;Winoto-Morbach, S;Uhlig, S
血小板活化因子（PAF）可诱导肺水肿，在急性肺损伤（ALI）中起关键作用。在这里，我们表明，PAF通过两种机制诱导肺水肿：酸性鞘磷脂酶（ASM）依赖的神经酰胺的生产，和环氧合酶途径的激活。干扰PAF诱导的神经酰胺合成的药物，如类固醇或黄原酸酯D609，可减轻PAF、内毒素或酸滴注诱导的肺水肿形成。我们的研究结果确定了酸性鞘磷脂酶和神经酰胺作为急性肺损伤的可能治疗靶点。
Platelet-activating factor (PAF) induces pulmonary edema and has a key role in acute lung injury (ALI). Here we show that PAF induces pulmonary edema through two mechanisms: acid sphingomyelinase (ASM)-dependent production of ceramide, and activation of the cyclooxygenase pathway. Agents that interfere with PAF-induced ceramide synthesis, such as steroids or the xanthogenate D609, attenuate pulmonary edema formation induced by PAF, endotoxin or acid instillation. Our results identify acid sphingomyelinase and ceramide as possible therapeutic targets in acute lung injury.