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目的：观察去乙酰化酶-1（SIRT1）对视网膜色素上皮细胞（RPE）氧化应激的防护作用。方法应用50μmol／L H2 O2与 ARPE-19细胞孵育24 h 诱导 RPE 产生氧化应激病理生理过程，观察细胞增殖及凋亡率、细胞活性氧水平（ROS），氧化剂诱导 RPE 细胞衰老状况，了解氧化应激对 RPE 的损伤；进一步采用 SIRT1激动剂白藜芦醇（RSV）及抑制剂烟酰胺（NA）分别处理经 H2 O2干预的 RPE 细胞，观察 SIRT1抗 RPE 氧化应激效果。结果①与对照组相比，H2 O2干预 RPE 后细胞增殖显著下降（P ＝0．020），凋亡率及内生 ROS 水平均显著增高（P ＝0．013，P ＝0．040），细胞衰老水平显著升高（P ＝0．045）；②NA 可显著提高 H2 O2的毒性作用，降低 RPE 细胞增殖率（P ＝0．049），刺激凋亡（P ＝0．028），使 ROS 累积和衰老速度增加；③RSV 具有显著的抗 H2 O2毒性作用；④RT-qPCR分析显示，SIRT1mRNA 水平显著下调。结论氧化应激状况下 SIRT1表达下调，表明 SIRT1对氧化应激诱发的视网膜色素上皮细胞损伤有显著的防护作用。适当提高 SIRT1活性也许是延缓 AMD 的一种治疗策略。“,”Objective To observe the protection role of the sirtuin 1 (SIRT1)towards the retinal pigmented epithelium (RPE)cells following exposure to oxidative stress.Methods The rates of proliferation and apoptosis,levels of intra-cellular reactive oxygen species(ROS)and cell senescence of RPEs,induced by oxidants (H2 O2 ),were evaluated. Results The results revealed a down-regulation of SIRT1 expression during oxidative stress.Furthermore,SIRT1 acti-vator resveratrol (RSV)and inhibitors nicotinamide (NA)were respectively treated on RPE cells following exposure by H2 O2 intervention;the expression of SIRT1 gene were detected by RT-PCR technology after RNA interfering on SIRT1.The experiments indicated that cell proliferation,apoptosis and ROS levels were significantly different compared with the control group after intervention by H2 O2 ,and cell senescence were significantly increased;NA was significant-ly increased the toxicity of H2 O2 ,however RSV had the opposite anti-cytotoxicity of H2 O2;RT-PCR analysis showed that SIRT1 levels were significantly reduced.Conclusion These results therefore suggested that down-regulation of SirT1 expression during oxidative stress,further investigation indicated that SIRT1 protected RPEs from oxidative stress-induced damage.Appropriate increase of the activity of SIRT1 may be a therapeutic strategy to delay AMD.