【摘要】 目的　证实阿司匹林的抗氧化作用是通过抑制一氧化氮 (NO)生成、增加铁蛋白 (Fn)表达来实现的。方法　在培养的内皮细胞中使用炎性因子诱导产生NO后 ,测定细胞中Fn的含量和细胞损伤的指标 ;观察不同浓度的阿司匹林 (AS)抑制NO产生后Fn及细胞损伤指标的改变和诱生型一氧化氮合酶 (iNOS)mRNA表达水平的变化。结果　诱导NO产生后 ,细胞Fn表达降低 ,细胞明显损伤 ;而低浓度的AS( 0 .3mmol/L)即可抑制 15 %的NO生成 ,增加细胞Fn的表达 ,同时能有效地对抗H2 O2 的损伤作用。随AS用量增加 ,抑制NO的作用渐增强。中小剂量 ( <10mmol/L)下AS对NO的抑制作用主要是在转录后水平影响iNOS的催化活性或蛋白表达 ,不影响iNOSmRNA水平 ;但高剂量的AS( 10mmol/L～ 2 0mmol/L)在转录水平上抑制iNOSmRNA的表达。水杨酸钠及消炎痛不具有抑制NO产生及诱导Fn表达的作用。结论　AS的抗氧化作用是通过抑制可诱导性NO产生 ,从而导致Fn表达增加来实现的。更多还原

【Abstract】 Objective To verify that the effects of aspirin resistance to oxidative damage were produced by suppressing inducible nitric oxide(NO) production and by increasing ferritin (Fn) synthesis in endothelial cells.Methods We observed the expression of ferritin and the effects of hydrogen peroxide toxicity toward cultured endothelial cells with inducible NO production. The index of cytotoxicity and the level of iNOS mRNA expression were measured when NO was suppressed by aspirin in variable concentration . Results After the production of inducible NO, a low expression of ferritin followed with significant toxicity toward cells. Aspirin with a low concentration (0.3 mmol/L) could reduce NO production by 15 %～20 % and increase the expression of Fn with an effective resistance against H 2O 2 damage. With the larger dose of AS, its efficacy was enhanced. Under a middle concentration(10 mmol/L) , aspirin was able to reduce enzymatic activity and protein expression at post-transcription level , followed by the steady state of iNOS mRNA level .Whereas , in a high concentration(10 mmol/L～20 mmol/L) , aspirin could increase the steady levels of iNOS mRNA .The other drugs such as salicylic acid and indomethacin failed to alter ferritin synthesis and NO inhibition.Conclusion These findings indicate that the mechanism of aspirin antioxidant has a direct relationship with suppressing inducible NO production, which will result in ferritin synthesis in endothelial cells.更多还原