title: Icariin inhibits corticosterone-induced apoptosis in hypothalamic neurons             via the PI3-K/Akt signaling pathway.
abstract: Excessive corticosterone (CORT) is acknowledged to induce neuronal damage             in a number of regions of the brain, particularly the hippocampus, the main area             implicated in depression. However, little research has been conducted on alterations             to hypothalamic neurons in depression and the cellular and molecular basis for             these changes. In the present study, we aimed to determine whether CORT causes             apoptosis in primary cultured hypothalamic neurons, and to investigate the protective             effects of icariin, an active natural ingredient from the Chinese plant, Epimedium             sagittatum Maxim. Our study demonstrates that exposure of hypothalamic neurons             to CORT causes a significant loss in viability, a significant decrease in mitochondrial             membrane potential, an increase in caspase-3 activity, an elevation in intracellular             reactive oxygen species elevation and decreased superoxide dismutase activity.             However, pretreatment of cells with icariin prior to CORT exposure was identified             to noticeably suppress these CORT-induced events. Furthermore, icariin may prevent             CORT-induced cell death via activation of the PI3-K/Akt pathway. In conclusion,             icariin is able to prevent CORT-induced hypothalamic cell apoptosis via activation             of the PI3-K/Akt pathway.
authors.affiliation: Laboratory of Lung, Inflammation and Cancers, Huashan Hospital, Fudan University, Shanghai 200040, PR China.
authors.forename: Hongying
authors.initials: H
authors.lastname: Zhang
authors.forename: Baojun
authors.initials: B
authors.lastname: Liu
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Wu
authors.forename: Changqing
authors.initials: C
authors.lastname: Xu
authors.forename: Jiang
authors.initials: J
authors.lastname: Tao
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Duan
authors.forename: Yuxue
authors.initials: Y
authors.lastname: Cao
authors.forename: Jingcheng
authors.initials: J
authors.lastname: Dong
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D002478:Cells, Cultured; D003345:Corticosterone / Q000494:pharmacology*; D034181:Epimedium / Q000737:chemistry; D005419:Flavonoids / Q000737:chemistry / Q000494:pharmacology*; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D005419:Flavonoids; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D053148:Caspase 3; C056599:icariin; D003345:Corticosterone