叶黄素对大鼠视网膜蓝光损伤防护作用机制研究

Molecular mechanism of the protective effect of lutein against retinal damage induced by blue-light in rats

目的探讨叶黄素防护视网膜蓝光损伤的相关机制。方法将大鼠按体重随机分为6组:正常对照组、模型对照组、溶剂对照组以及叶黄素低、中、高剂量组。叶黄素低、中、高剂量组分别注射0.5、1.0和2.0mg/ml的叶黄素,溶剂对照组注射由生理盐水和Tween80以9:1混合的溶剂,注射剂量均为5μl。暗适应24h,利用蓝光光损伤仪建立大鼠视网膜光损伤模型,光暴露时间为2h。光暴露结束后暗适应72h,处死取视网膜测定氧化应激指标、神经元型一氧化氮合酶(nNOS)和c-fos蛋白的表达情况。结果与模型对照组及溶剂对照组相比,叶黄素剂量组大鼠视网膜中丙二醛(MDA)含量显著减少(P<0.05),而SOD和GSH-Px的活性在各组间差异无显著性。叶黄素剂量组大鼠视网膜中c-fos蛋白的表达量低于溶剂对照组和模型对照组(P<0.05),而nNOS的表达量与其他组相比差异无显著性(P>0.05)。结论叶黄素可能通过淬灭氧自由基,抑制脂质过氧化和c-fos基因的表达发挥其保护作用。

Objective To explore the possible mechanisms of the protective effect of lutein against retinal damage induced by blue-light.Methods Ninety six female SD rats（8 week-old,200g） were divided into six groups：normal control（NC）,blue light injury（MC）,blue light ＋ solvent（SC）,blue light ＋ 0.5mg /ml lutein（L0.5）,blue light ＋ 1.0mg/ml lutein（L1.0） and blue light ＋ 2.0mg/ml lutein（L2.0）.The content of malondialdehyde（MDA） and the activities of peroxide dismutase（SOD） and glutathione peroxidase（GSH-Px） of retina were measured as oxidative stress markers.Neuron nitricoxide synthase and the expression of c-fos protein in retina were analyzed by Western Blot.Results The content of MDA increased in the retina induced by photic injury,and the increase was protected significantly by lutein treatment（P 0.05）,but no dose-dependent response of lutein on the activities of SOD and GSH-Px was observed（P 0.05）.The expression of c-fos protein was significantly higher in the retina of MC and SC group than that in lutein-treated groups（P 0.05）,while the expression of nNOS was not significant different between groups.Conclusion The mechanisms of lutein protecting retina from blue-light damage might be quenching singlet oxygen,inhibiting lipid peroxidation and c-fos gene expression.