【摘要】 目的　探讨阿司匹林 (AS)抗氧化作用的机制。方法　观察不同浓度的 AS在抗 H2 O2 损伤内皮细胞过程中诱导铁蛋白 (Fn)表达的情况 ,以及添加外源性 Fe Cl3 和细胞内铁螯合剂去铁胺时对 AS诱导 Fn表达的影响。结果　极低剂量 (0 .1m mol/ L)的 AS即可诱导内皮细胞 Fn表达超过对照 2 5 % (P<0 .0 5 ) ,使乳酸脱氢酶(L DH)释放率减少 5 0 % ,保护 74.4%的细胞避免 H2 O2 的损伤 ,同时使氧自由基指标丙二醛明显下降。AS与 Fn表达之间表现出剂量与时间依赖关系 ,且对细胞的保护作用逐渐增强。但使用去铁胺去除细胞内游离铁能明显降低AS诱导 Fn表达的作用 ,而加入 Fe Cl3 后诱导 Fn表达的作用增强。结论　初步证实 AS的抗氧化作用是通过影响细胞内铁代谢变化 ,增加 Fn表达实现的更多还原

【Abstract】 Objective To explore the mechanism of aspirin for resistance to oxidative damage in endothelial cells. Methods Using cultured endothelial cells, we measured the levels of aspirin induced ferritin expression on resistance to hydrogen peroxide toxicity toward cells in the presence of the iron chelator desferrioxamine added to FeCl 3. Results Aspirin at low concentration (0.1mmol/L) induced significant increase of ferritin expression in a time and concentration dependent fashion up to 25% over basal levels( P <0.05). Preincubating the cells for 8h with aspirin (0.1mmol/L) reduced lactate dehydrogenase( LDH) release rate by 50%, toxicity reduction by 40%, and significant decrease of malondialdehyde (MDA) production. Aspirin induced cytoprotection from H 2O 2 damage was also in a concentration and time dependent fashion. However, in the presence of the iron chelator desferrioxamine, aspirin enhanced ferritin synthesis was abrogated, in contrast, FeCl 3 increased aspirin induced ferritin synthesis in cells. Conclusion The study suggested that the antioxidation of aspirin was brought into action by affecting the cellular iron metabolism pathway to induce ferritin synthesis.更多还原