Shen Y H, Wang X L, Wilcken D E
Department of Cardiovascular Medicine, University of New South Wales, Prince of Wales Hospital, Randwick, Australia.
FEBS Lett. 1998 Aug 14;433(1-2):125-31. doi: 10.1016/s0014-5793(98)00844-8.
Physiological levels of nitric oxide (NO) regulate vascular tone and protect the microvasculature from injury whereas excessive NO may be harmful. The present study explored the effects of NO on human endothelial cell apoptosis. We found that the NO donor S-nitroso-N-acetylpenicillamine (SNAP) inhibited TNFalpha-induced endothelial apoptosis and that this was mediated partly through the cGMP pathway. In contrast, high SNAP concentration induced endothelial apoptosis via cGMP-independent pathways and the cGMP pathway protected against NO-induced apoptosis. These findings demonstrate that low NO concentrations contribute to human endothelial cell survival, whereas higher NO concentrations are pathological and promote destruction of endothelial cells.
生理水平的一氧化氮（NO）调节血管张力并保护微血管免受损伤，而过量的NO可能有害。本研究探讨了NO对人内皮细胞凋亡的影响。我们发现NO供体S-亚硝基-N-乙酰青霉胺（SNAP）抑制肿瘤坏死因子α（TNFα）诱导的内皮细胞凋亡，且这部分是通过环磷酸鸟苷（cGMP）途径介导的。相反，高浓度的SNAP通过不依赖cGMP的途径诱导内皮细胞凋亡，而cGMP途径可防止NO诱导的凋亡。这些发现表明，低浓度的NO有助于人内皮细胞存活，而较高浓度的NO具有病理学意义并促进内皮细胞的破坏。
