目的：探究间歇性禁食(intermittent fasting, IF)对内毒素诱导小鼠葡萄膜炎(endotoxin-induced uveitis, EIU)的保护作用及其可能的抗炎机制。方法：小鼠随机分为对照组(Ctr)、EIU组及IF+EIU组。16∶8禁食方案(9 : 00—17 : 00进食)。对照组行玻璃体腔内注射磷酸盐缓冲溶液(phosphate buffered saline, PBS)，其余两组行玻璃体腔内脂多糖注射。建模后监测小鼠空腹血糖及体质量。光学相干断层扫描和苏木精伊红染色观察评估炎症水平。视网膜铺片行神经炎症相关的观察评价。BV2细胞分为Ctr组，LPS组及饥饿+内毒素组，蛋白印迹及实时荧光定量逆转录PCR技术检测相关蛋白及mRNA表达水平。结果：①IF对体质量无明显影响，可引起血糖显著降低随后逐渐恢复。病程中期起IF干预下小鼠视网膜水肿恢复，玻璃体腔内炎性渗出比EIU组显著减少(P＜0.01)。IF逆转LPS诱导的小胶质细胞激活，减轻视网膜神经节细胞及神经纤维损伤(P＜0.05)。②饥饿培养抑制LPS诱导的BV2细胞的磷酸化信号转导与转录激活因子1和3及诱导型一氧化氮合酶( inducible nitric oxide synthase, iNOS)的蛋白表达水平(P＜0.05)，显著降低iNOS、白介素-6等炎症因子的表达水平。结论：IF能够加速EIU炎症的消退，减轻组织结构的炎性破坏，抑制小胶质细胞的促炎型激活。

Objective: To investigate the protective effects of intermittent fasting (IF) on endotoxin-induced uveitis in mice and its potential anti-inflammatory mechanisms. Methods: Mice were randomly divided into three groups: control group (Ctr), endotoxin-induced uveitis (EIU) group, and IF + EIU group. The IF regimen followed a 16:8 fasting scheme (feeding from 9:00 to 17:00). The control group received intravitreal injections of PBS, while the other two groups received intravitreal injections of lipopolysaccharide (LPS). After modeling, fasting blood glucose and body weight of the mice were monitored. Inflammation levels were assessed using OCT and H&E staining. Retinal flat mounts were used for evaluating neuroinflammation. BV2 cells were divided into Ctr group, LPS group, and starvation (LG) + LPS group. The expression levels of related proteins and mRNA were detected using WB and RT-qPCR. Results: IF had no significant effect on body weight but caused a significant decrease in blood glucose, which gradually recovered. From the middle stage of the disease, mice in the IF intervention group show edretinal edema recovery, significantly reduced intravitreal inflammatory exudation and cell infiltration compared to the EIU group (P <0.01). IF reversed LPS-induced microglial activation and significantly alleviated damage to retinal ganglion cells and nerve fibers (P <0.05). Starvation culture significantly inhibited LPS-induced expression levels of p-STAT1/3 and iNOS proteins in BV2 cells (P <0.05) and significantly reduced the expression levels of inflammatory factors such as iNOS and IL-6. Conclusion: IF can accelerate the resolution of EIU inflammation, reduce inflammatory damage to tissue structures, and inhibit pro-inflammatory activation of microglia.