叶黄素对D-半乳糖致氧化损伤小鼠HO-1、TLR4表达的影响

Effect of lutein on relieving oxidative stress in mice induced by D-galatose

目的研究叶黄素缓解D-半乳糖诱导小鼠氧化应激损伤的作用机制。方法 48只昆明种小鼠随机分为D-半乳糖模型对照组、叶黄素低剂量组(10mg/kg·d)、叶黄素高剂量组(40mg/kg·d)和正常对照组。6周后观察小鼠肝组织活性氧(ROS)、一氧化氮(NO)含量,总一氧化氮合酶(TNOS)、诱导型一氧化氮合酶(iNOS)和线粒体ATP酶(ATPase)活性,RT-PCR法检测血红素氧合酶(HO-1)和toll样受体4(TLR4)mRNA表达水平。结果叶黄素低、高剂量组小鼠肝组织ROS含量低于模型对照组(P<0.01);低、高剂量组线粒体Na+-K+-ATP酶及高剂量组线粒体Ca2+-ATP酶活性高于模型对照组(P<0.05);高剂量组TNOS、iNOS活性及NO含量低于模型对照组(P<0.05);高剂量组小鼠肝HO-1mRNA表达高于模型对照组(P<0.05),叶黄素低、高剂量组TLR4mRNA表达均低于模型对照组(P<0.01)。结论叶黄素降低D-半乳糖小鼠氧化应激效应可能与其提高HO-1表达和下调TLR4mRNA表达有关。

Objective To study the effect of lutein on relieving oxidative stress in the liver of mice induced by D-galactose（D-gal）.Methods Forty eight Kunming strain mice were randomized into 4 groups： model group,low lutein group （LL 10 mg /（kg·d））,high lutein group（HL 40 mg /（kg·d）） and normal control group.The content of reactive oxygen species （ROS）,nitric oxide （NO） and activity of total nitric oxide synthase （TNOS）,inducible nitric oxide synthase （ iNOS） and mitochondrial Na ^＋ -K^ ＋ -ATPase,Ca^2 ＋ -ATPase in liver tissue were detected 6 weeks later in the experiment.The expression of toll-like receptor-4 （TLR4） mRNA and hemeoxygenase-1 （HO-1） mRNA in hepatic tissue were detected by reverse transcription polymerase chain reaction （ RT-PCR） technique.Results ROS content in HL and LL group was significantly lower（P〈0.01） than that in the model group.The activity of Na ^＋ - K^ ＋ -ATPase in HL and LL group and the activity of Ca^2 ＋ -ATPase in HL group were significantly higher than that in the model group （ P〈0.05）.The activities of TNOS and iNOS and the content of NO in HL group were significantly lower than the model group （P〈0.05）.The expression of HO-1 mRNA in HL group was significantly higher than that in the model group,but the expression of TLR4 mRNA in HL group was significantly lower than that in the model group （ P〈0.05）.Conclusion The mechanism of lutein on the protection of mice from oxidative stress induced by D-gal might be related to increasing the expression of HO-1 mRNA and reducing the expression of TLR4 mRNA.