详细信息
Treatment with lutein provides neuroprotection in mice subjected to transient cerebral ischemia ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Treatment with lutein provides neuroprotection in mice subjected to transient cerebral ischemia
作者:Sun, Ya-Xuan[1];Liu, Ting[2];Dai, Xue-Ling[1];Zheng, Qiu-Sheng[2];Hui, Bo-Di[1];Jiang, Zhao-Feng[1]
第一作者:孙雅煊
通讯作者:Jiang, ZF[1]
机构:[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Shihezi Univ, Sch Pharm, Minist Educ, Key Lab Xinjiang Endem Phytomed Resources, Shihezi 832002, Peoples R China
第一机构:北京联合大学应用文理学院|北京联合大学生物化学工程学院
通讯机构:[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China.|[114172]北京联合大学应用文理学院;[11417]北京联合大学;[1141726]北京联合大学生物化学工程学院;
年份:2014
卷号:16
期号:11
起止页码:1084-1093
外文期刊名:JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
收录:;Scopus(收录号:2-s2.0-84911953710);WOS:【SCI-EXPANDED(收录号:WOS:000344594100007)】;
语种:英文
外文关键词:oxidative stress; lutein; neuroprotection; antioxidant; transient cerebral ischemia
摘要:Lutein is known to be a nonprovitamin A carotenoid found in broccoli and spinach. The aim of present study was to investigate whether lutein can protect brain against ischemic injury by reducing oxidative stress. Male ICR mice were randomly divided into five experimental groups: model group, sham group, lutein high, middle, and low-dose groups (30, 15, and 7.5mg/kg). Mice were subjected to a 2-h middle cerebral artery occlusion followed by reperfusion for 22h. The reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, antioxidant enzyme activities, malondialdehyde (MDA), and the carbonyl content in oxidatively modified proteins in brain tissue were determined with colorimetric method. The 8-hydroxy deoxyguanosine (8-OHdG) expression was measured by immunohistochemistry assay, and the neuron apoptosis was detected by TdT-mediated dUTP nick end labeling assay. Then, the neurological deficit scores were measured at last. Treatment of lutein significantly elevated the ratio of GSH/GSSG as well as activities of superoxide dismutase, glutathione peroxidase, and catalase and obviously decreased the contents of MDA, brain carbonyl, the expression of 8-OHdG, the number of apoptotic cells, and neurological deficit scores. Our results demonstrate that administration of lutein affords strong neuroprotective effect against transient cerebral ischemic injury and that the effect might be associated with its antioxidant property.
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