Schizandrin prevents dexamethasone-induced cognitive deficits  

作　　者：Xiao Xu Xing Zhou Xiao-Wen Zhou Zheng Zhang Min-Jing Liao Qi Gao Huan-Min Luo 

机构地区：[1]Department of Pharmacology, School of Medicine, Jinan University, Guangzhou 510632, China [2]Department of Physiology, School of Medicine, Henan University, Kaifeng 475000, China [3]The Joint Laboratory of Brain Function and Health, Jinan University and the University of Hong Kong, Jinan University, Guangzhou 510632, China

出　　处：《Neuroscience Bulletin》2012年第5期532-540,共9页神经科学通报（英文版）

基　　金：supported by grants from the National Basic Research Development program (973 Program) of China (2011CB707500);the National Natural Science Foundation of China (81173037 and 30672450);the Scientific program of Department of Science and Technology, Guangdong Province, China(2010B030700018)

摘　　要：Objective To model glucocorticoid-induced cognitive impairment and evaluate the neuroprotection by schi-zandrin （Sch） against dexamethasone （Dex）-induced neurotoxicity in vivo and in vitro. Methods Cerebral cortical cells from neonatal Sprague-Dawley rats （within 24 hours after birth） were cultured for 9 days, and then treated with Dex （10 -4 , 10 -5 , 10 -6 or 10 -7 mol/L） for 24 h or pretreated with 10 -4 mol/L Dex for 24 h followed by 10, 20, 40, or 80 μmol/L Schfor 48 h. Cell viability was assessed using the MTT assay. Immunofluorescence and real-time PCR for MAP2 were performed to confirm the effects of Dex on neurite outgrowth. In vivo, kunming mice were randomly divided into six groups： control [（intragastric （i.g.） vehicle for 42 days]; Dex group I （5 mg/kg·d -1 Dex i.g. treatment for 28 days followed by i.g. vehicle for 14 days）; Dex group II （Dex i.g. for 42 days）; Dex ＋ Sch （Dex i.g. for 28 days followed by 5, 15, or 45 mg/kg·d -1 Sch i.g. for 14 days）. Learning and memory were assessed by Morris water maze test. Histological examination was used to assess pathology and apoptosis in neurons. Results Compared to the Dex groups, Sch increased cell viability in a dose-dependent manner, improved performance in the Morris water maze and ameliorated the morphological changes. Conclusion Sch has neuroprotective effects against insults induced by glucocorticoid.Objective To model glucocorticoid-induced cognitive impairment and evaluate the neuroprotection by schi-zandrin （Sch） against dexamethasone （Dex）-induced neurotoxicity in vivo and in vitro. Methods Cerebral cortical cells from neonatal Sprague-Dawley rats （within 24 hours after birth） were cultured for 9 days, and then treated with Dex （10 -4 , 10 -5 , 10 -6 or 10 -7 mol/L） for 24 h or pretreated with 10 -4 mol/L Dex for 24 h followed by 10, 20, 40, or 80 μmol/L Schfor 48 h. Cell viability was assessed using the MTT assay. Immunofluorescence and real-time PCR for MAP2 were performed to confirm the effects of Dex on neurite outgrowth. In vivo, kunming mice were randomly divided into six groups： control [（intragastric （i.g.） vehicle for 42 days]; Dex group I （5 mg/kg·d -1 Dex i.g. treatment for 28 days followed by i.g. vehicle for 14 days）; Dex group II （Dex i.g. for 42 days）; Dex ＋ Sch （Dex i.g. for 28 days followed by 5, 15, or 45 mg/kg·d -1 Sch i.g. for 14 days）. Learning and memory were assessed by Morris water maze test. Histological examination was used to assess pathology and apoptosis in neurons. Results Compared to the Dex groups, Sch increased cell viability in a dose-dependent manner, improved performance in the Morris water maze and ameliorated the morphological changes. Conclusion Sch has neuroprotective effects against insults induced by glucocorticoid.

关 键 词：NEURON GLUCOCORTICOID cognitive impairment 

分 类 号：Q95-33[生物学—动物学] S858.237.2[农业科学—临床兽医学]