TY - DATA T1 - The role of histone deacetylase inhibitors in regulation of Akt/GSK-3β signaling pathway in mice following transient focal cerebral ischemia PY - 2017/12/05 AU - Bo Zhao AU - Lian Liu AU - Yan Leng AU - Quan Yuan AU - Jiabao Hou AU - Yang Wu AU - Wenwei Gao UR - https://scielo.figshare.com/articles/dataset/The_role_of_histone_deacetylase_inhibitors_in_regulation_of_Akt_GSK-3_signaling_pathway_in_mice_following_transient_focal_cerebral_ischemia/5666221 DO - 10.6084/m9.figshare.5666221.v1 L4 - https://ndownloader.figshare.com/files/9888196 L4 - https://ndownloader.figshare.com/files/9888202 L4 - https://ndownloader.figshare.com/files/9888208 L4 - https://ndownloader.figshare.com/files/9888211 L4 - https://ndownloader.figshare.com/files/9888223 L4 - https://ndownloader.figshare.com/files/9888241 L4 - https://ndownloader.figshare.com/files/9888250 KW - Histone Deacetylases KW - Glycogen Synthase Kinase 3 beta KW - Brain Ischemia KW - Reperfusion Injury KW - Mice N2 - Abstract Purpose: To investigate whether the neuroprotective effect of TSA on cerebral ischemia reperfusion injury is mediated by the activation of Akt/GSK-3β signaling pathway. Methods: Mice were randomly divided into four groups (n=15): sham group (S); ischemia reperfusion group (IR); ischemia reperfusion and pretreated with TSA group (IR+T); ischemia reperfusion and pretreated with TSA and LY294002 group (IR+T+L). The model of cerebral ischemia reperfusion was established by 1h of MCAO following 24h of reperfusion. TSA (5mg/kg) was intraperitoneally given for 3 days before MCAO, Akt inhibitor, LY294002 (15 nmol/kg) was injected by tail vein 30 min before the MCAO. Results: TSA significantly increased the expression of p-Akt, p-GSK-3β proteins and the levels of SOD, Bcl-2, reduced the infarct volume and the levels of MDA, ROS, TNF-α, IL-1β, Bax, Caspase-3, TUNEL and attenuated neurological deficit in mice with transient MCAO, LY294002 weakened such effect of TSA dramatically. Conclusions: TSA could significantly decrease the neurological deficit and reduce the cerebral infarct volume, oxidative stress, inflammation, as well as apoptosis during cerebral ischemia reperfusion injury, which was achieved by activation of the Akt/GSK-3β signaling pathway. ER -