文献类型：期刊文献

英文题名：Neuroprotective effects of liquiritin on cognitive deficits induced by soluble amyloid-beta(1-42) oligomers injected into the hippocampus

作者：Jia, Shi-Liang[1];Wu, Xue-Ling[1];Li, Xiao-Xiao[1];Dai, Xue-Ling[1];Gao, Zhao-Lan[1];Lu, Zheng[1];Zheng, Qiu-Sheng[2];Sun, Ya-Xuan[1]

第一作者：Jia, Shi-Liang

通讯作者：Sun, YX[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Binzhou Med Univ, Sch Chinese Med Integrated Western Med, Yantai 264003, Peoples R China

第一机构：北京联合大学生物化学工程学院|北京联合大学应用文理学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;[114172]北京联合大学应用文理学院;

年份：2016

卷号：18

期号：12

起止页码：1186-1199

外文期刊名：JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000385839800010)】；

基金：This work was supported by the Scientific Research Common Program of Beijing Municipal Commission of Education [grant number SQKM201411417014]; the Beijing Union University Campus Project [grant number zk70201402].

语种：英文

外文关键词：Liquiritin; alzheimer's disease; amyloid-beta(1-42); oxidative stress; apoptosis

摘要：This study assessed the modulating effects of liquiritin against cognitive deficits, oxidative damage, and neuronal apoptosis induced by subsequent bilateral intrahippocampal injections of aggregated amyloid-(1-42) (A(1-42)). This study also explored the molecular mechanisms underlying the above phenomena. Liquiritin was orally administered to rats with A(1-42)-induced cognitive deficits for 2weeks. The protective effects of liquiritin on the learning and memory impairment induced by A(1-42) were examined in vivo by using Morris water maze. The rats were then euthanized for further studies. The antioxidant activities of liquiritin in the hippocampus of the rats were investigated by biochemical and immunohistochemical methods. The apoptosis of the neurons was assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling assay. Liquiritin at doses of 50-100mg/kg significantly improved the cognitive ability, restored the abnormal activities of glutathione peroxidase and superoxide dismutase, and decreased the levels of malondialdehyde,8-hydroxy-2-deoxyguanosine and protein carbonyl in the hippocampus of rats with Alzheimer's disease. Moreover, neural apoptosis in the hippocampus of A(1-42)-treated rats was reversed by liquiritin. Liquiritin can significantly ameliorate A(1-42)-induced spatial learning and memory impairment by inhibiting oxidative stress and neural apoptosis.