N-acetyl-cysteine attenuates endotoxin-induced adhesion molecule expression in human whole blood

N-acetyl-cysteine attenuates endotoxin-induced adhesion molecule expression in human whole blood
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DOI:
10.1213/01.ane.0000148616.24996.e7
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发表时间:
2005-05-01
影响因子:
5.7
通讯作者:
Shigematsu, A
Shigematsu, A
中科院分区:
医学2区
文献类型:
--
作者:
Nandate, K;Ogata, M;Shigematsu, A

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白细胞粘附内皮细胞在内毒素休克早期起关键作用。白细胞对内毒素反应的减弱可能有助于防止进一步的器官功能障碍。最近的证据表明,n-乙酰半胱氨酸(NAC)减弱内毒素引起的病理生理变化。我们研究了NAC对内毒素刺激的人全血CD11b和CD62L表达的影响。NAC (bbb10 mM)以浓度依赖的方式显著抑制脂多糖(LPS)诱导的CD11b上调。然而,NAC不影响lps诱导的CD62L下调。我们还分析了NAC对白细胞介素-8 (IL-8)诱导的人全血CD11b表达的影响。IL-8 (10 ng/mL)显著上调CD11b的表达,NAC (bbb10 mM)显著减弱IL-8诱导的上调,且呈剂量依赖性。我们得出结论,NAC减弱了LPS或il -8刺激的人全血中CD11b的表达。
Leukocyte adhesion to endothelial cells plays a pivotal role in the early stage of endotoxin shock. The attenuation of the leukocyte response to endotoxin may contribute to the prevention of further organ dysfunction. Recent evidence implies that N-acetyl-cysteine (NAC) attenuates endotoxin-induced pathophysiological changes. We investigated the effect of NAC on the expression of CD11b and CD62L in endotoxin-stimulated human whole blood. NAC (> 10 mM) significantly inhibited the lipopolysaccharide (LPS)-induced upregulation of CD11b in a concentration-dependent manner. However, NAC did not affect the LPS-induced downregulation of CD62L. We also analyzed the effect of NAC on interleukin-8 (IL-8)induced expression of CD11b in human whole blood. IL-8 (10 ng/mL) significantly upregulated the expression of CD11b, and the IL-8-induced upregulation was significantly attenuated by NAC (> 10 mM) in a dose-dependent manner. We conclude that NAC attenuates the increased expression of CD11b in either LPS or IL-8-stimulated human whole blood.