眼科新进展2025，Vol.45Issue(11)：859-863,5.DOI:10.13389/j.cnki.rao.2025.0148
抗氧化物莱视盯对氢醌诱导的干性年龄相关性黄斑变性模型小鼠的保护作用及其机制
The protective effect and mechanism of antioxidant Lutein in a mouse model of hydroquinone-induced dry age-related macular degeneration
摘要
Abstract
Objective To investigate the protective effect and mechanism of the antioxidant Lutein in a mouse model of dry age-related macular degeneration(AMD)induced by hydroquinone.Methods Twenty-four specific pathogen-free(SPF)grade male C57BL/6 mice,aged 6-8 weeks,were randomly divided into 3 groups(n=8 per group).The control group was fed a standard diet and water for 3 months.The model group and the drug intervention group received 8 g·L-1 hydroquinone in drinking water combined with a high-fat diet for 2 months to establish the dry AMD mouse model.After modeling,the model group resumed a standard diet and water for 1 month.The drug group received oral gavage daily at 8:00 AM,administered Lutein at 0.1 g per kg body weight(dissolved in distilled water),for 1 month.At the experimental endpoint,all mice were euthanized,and samples were collected for analysis.The ultrastructure of retinal pigment epithelial(RPE)cells was observed by electron microscopy.Serum activities of superoxide dismutase(SOD),catalase(CAT),and glutathione peroxidase(GSH-Px)were measured using a microplate reader.mRNA expression levels of nuclear factor ery-throid 2-related factor 2(Nrf2),heme oxygenase-1(HO-1),and glutamate-cysteine ligase(GCL)in retinal tissue were de-tected by real-time quantitative PCR.Protein expression levels of Nrf2,HO-1,and GCL in retinal tissue were determined by Western blot.Results In the model group,mitochondria and intracellular organelles in RPE cells exhibited vacuolar de-generation,with compromised structural integrity;simultaneously,microvilli were disorganized and significantly reduced in number.In the drug group,the mitochondrial structure of RPE cells was relatively well-preserved,with morphology largely normal;microvilli structure was clear,and density showed some recovery compared to the model group.Compared to the control group,serum activities of SOD,CAT,and GSH-Px were significantly decreased in the model group(all P＜0.01).Compared to the model group,serum activities of SOD,CAT,and GSH-Px were significantly increased in the drug group(all P＜0.05).Compared to the control group,retinal mRNA expression levels of Nrf2,HO-1,and GCL were significantly decreased in the model group(all P＜0.01).Compared to the model group,retinal mRNA expression levels of Nrf2,HO-1,and GCL were significantly increased in the drug group(all P＜0.01).Compared to the control group,retinal protein ex-pression levels of Nrf2,HO-1,and GCL were decreased in the model group(all P＜0.05).Compared to the model group,retinal protein expression levels of Nrf2,HO-1,and GCL were increased in the drug group(all P＜0.05).Conclusion The antioxidant Lutein promotes the expression of downstream target genes HO-1 and GCL by activating the Nrf2 signaling pathway,which not only enhances the biosynthesis levels of antioxidant enzymes(SOD,CAT,GSH Px),but also effec-tively inhibits oxidative stress response by enhancing autophagic activity.关键词
抗氧化物/莱视盯/Nrf2通路/氢醌/干性年龄相关性黄斑变性/视网膜氧化损伤Key words
antioxidants/Lutein/Nrf2 pathway/hydroquinone/dry age-related macular degeneration/retinal oxida-tive damage分类
临床医学引用本文复制引用
张阳,单婷婷,唐敏,李嘉愔,任静..抗氧化物莱视盯对氢醌诱导的干性年龄相关性黄斑变性模型小鼠的保护作用及其机制[J].眼科新进展,2025,45(11):859-863,5.基金项目
广东省中医药局科研项目(编号:20231024) （编号:20231024）
广东省第二中医院科研项目(编号:SEZYY2024C01) （编号:SEZYY2024C01）
