Sundaresan M, Yu Z X, Ferrans V J, Irani K, Finkel T
Cardiology Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD 20892-1650, USA.
Science. 1995 Oct 13;270(5234):296-9. doi: 10.1126/science.270.5234.296.
Stimulation of rat vascular smooth muscle cells (VSMCs) by platelet-derived growth factor (PDGF) transiently increased the intracellular concentration of hydrogen peroxide (H2O2). This increase could be blunted by increasing the intracellular concentration of the scavenging enzyme catalase or by the chemical antioxidant N-acetylcysteine. The response of VSMCs to PDGF, which includes tyrosine phosphorylation, mitogen-activated protein kinase stimulation, DNA synthesis, and chemotaxis, was inhibited when the growth factor-stimulated rise in H2O2 concentration was blocked. These results suggest that H2O2 may act as a signal-transducing molecule, and they suggest a potential mechanism for the cardioprotective effects of antioxidants.
血小板衍生生长因子(PDGF)刺激大鼠血管平滑肌细胞(VSMC)会使细胞内过氧化氢(H2O2)浓度短暂升高。增加细胞内清除酶过氧化氢酶的浓度或使用化学抗氧化剂N-乙酰半胱氨酸可减弱这种升高。当生长因子刺激引起的H2O2浓度升高被阻断时,VSMC对PDGF的反应(包括酪氨酸磷酸化、丝裂原活化蛋白激酶刺激、DNA合成和趋化性)受到抑制。这些结果表明,H2O2可能作为一种信号转导分子,并且提示了抗氧化剂心脏保护作用的潜在机制。