Analysis of the reactive oxygen species (ROS)-detoxifying biomarkers may elucidate the mitochondrial dysfunction in glaucoma pathogenesis. Therefore, we purposed to investigate the effects of ROS-detoxifying molecules including Silent Information Regulator T1 (SIRT1) and Forkhead Box O 1 (FOXO1) and 3a (FOXO3a) transcription factors in patients with glaucoma. Our analyses included 20 eyes from patients with primary open-angle glaucoma (POAG) and 20 eyes from patients with pseudoexfoliation glaucoma (PXG) who were scheduled for trabeculectomy. After extraction of total RNA from trabecular meshwork tissue, we compared the levels of SIRT1, FOXO1and FOXO3a genes in the oxidative pathway with the level of glyceraldehyde-3 phosphate dehydrogenase (GAPDH), the reference gene, using real-time polymerase chain reaction. Relative gene expression was calculated using the threshold cycle (2^−ΔΔCT) method. We observed similarly reduced expression levels of SIRT1, FOXO1, and FOXO3a genes versus GAPDH among patient groups (p = 0.40; p = 0.56; p = 0.35, respectively). This is the first study to identify the role of SIRT1 and FOXOs in human TM with glaucoma. Relative expression levels of SIRT1, FOXO1, and FOXO3a genes versus a control gene (GAPDH) were decreased in POAG and PXG groups. Our results show that SIRT1and FOXOs (1-3a) deserve special attention in the pathogenesis of glaucoma.

分析活性氧（ROS）的解毒生物标志物可以阐明青光眼发病机理中的线粒体功能障碍。因此，我们旨在研究ROS解毒分子（包括沉默信息调节剂T1 （SIRT1）和叉头箱O 1（FOXO1）和3a（FOXO3a）转录因子）在青光眼患者中的作用。我们的分析包括计划进行小梁切除术的原发性开角型青光眼（POAG）患者的20眼和假脱落性青光眼（PXG）患者的20眼。从小梁网组织中提取总RNA后，我们比较了SIRT1，FOXO1和FOXO3a的水平这些基因在氧化途径中的水平与甘油三磷酸甘油醛脱氢酶（GAPDH）的水平有关，作为参考基因，采用实时聚合酶链反应。使用阈值循环（2- ^ΔΔCT）方法计算相对基因表达。我们观察到患者组中SIRT1，FOXO1和FOXO3a基因的表达水平相对于GAPDH的降低程度相似（分别为p = 0.40； p = 0.56； p = 0.35）。这是鉴定SIRT1和FOXO在青光眼人类TM中的作用的第一项研究。SIRT1，FOXO1和FOXO3a基因相对于对照基因的相对表达水平（POAG和PXG组的GAPDH）降低。我们的结果表明，SIRT1和FOXOs（1-3a）在青光眼的发病机理中值得特别注意。