Lipopolysaccharides (LPS)-induced retinal inflammation is an important factor in retinal diseases. This study was aimed to investigate the effect of Sirt6 on LPS-induced retinal injury. ARPE-19 cells were incubated with LPS to induce inflammation. The cell viability was determined using CCK-8 assay. The mRNA level and protein expression of corresponding genes was detected using qRT-PCR and western blot, respectively. The production of inflammatory cytokines was measured using ELISA kit. The levels of oxidative stress-related factors were measured using their detection kits. Cell apoptosis was observed using TUNEL assay. The results showed that Sirt6 was downregulated after LPS treatment. Sirt6 strengthened LPS-induced autophagy by promoting the expression of LC3II/I, beclin1 and ATG5. Sirt6 treatment significantly inhibited LPS-induced inflammation, oxidative stress and cell apoptosis, which was then partly abolished by 3 MA. These results suggest Sirt6 to be an important regulator for LPS-induced inflammation, oxidative stress, and apoptosis partly by regulating cell autophagy.

脂多糖（LPS）引起的视网膜炎症是视网膜疾病的重要因素。这项研究旨在调查Sirt6对LPS诱导的视网膜损伤的影响。将ARPE-19细胞与LPS孵育以诱导炎症。使用CCK-8测定法测定细胞活力。分别使用qRT-PCR和western blot检测相应基因的mRNA水平和蛋白质表达。使用ELISA试剂盒测量炎性细胞因子的产生。使用其检测试剂盒测量了氧化应激相关因子的水平。使用TUNEL测定法观察到细胞凋亡。结果表明，LPS处理后Sirt6被下调。Sirt6通过促进LC3II / I，beclin1和ATG5的表达增强LPS诱导的自噬。Sirt6处理可显着抑制LPS诱导的炎症，氧化应激和细胞凋亡，然后在3 MA中被部分清除。这些结果表明，Sirt6是LPS诱导的炎症，氧化应激和细胞凋亡的重要调节剂，部分是通过调节细胞自噬来实现的。