血小板活化因子介导的肺水肿：酸性鞘磷脂酶和神经酰胺的新作用。
PAF-mediated pulmonary edema: a new role for acid sphingomyelinase and ceramide.
作者信息
Göggel Rolf, Winoto-Morbach Supandi, Vielhaber Gabriele, Imai Yumiko, Lindner Karsten, Brade Lore, Brade Helmut, Ehlers Stefan, Slutsky Arthur S, Schütze Stefan, Gulbins Erich, Uhlig Stefan
机构信息
Research Center Borstel, Leibniz Center for Medicine and Biosciences, 23845 Borstel, Germany.
出版信息
Nat Med. 2004 Feb;10(2):155-60. doi: 10.1038/nm977. Epub 2004 Jan 4.
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.
血小板活化因子（PAF）可诱发肺水肿，在急性肺损伤（ALI）中起关键作用。我们在此表明，PAF通过两种机制诱发肺水肿：酸性鞘磷脂酶（ASM）依赖性神经酰胺生成以及环氧合酶途径的激活。干扰PAF诱导的神经酰胺合成的药物，如类固醇或黄原酸盐D609，可减轻PAF、内毒素或酸灌注诱导的肺水肿形成。我们的研究结果确定酸性鞘磷脂酶和神经酰胺可能是急性肺损伤的治疗靶点。
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