There is no effective drug to treat Alzheimer＇s disease （AD）, a neurodegenerative disease affecting an estimated 30 million people around the world. Strongly supported by preclinical and clinical studies, amyloid-b...There is no effective drug to treat Alzheimer＇s disease （AD）, a neurodegenerative disease affecting an estimated 30 million people around the world. Strongly supported by preclinical and clinical studies, amyloid-beta （Aβ） may be a target for developing drugs against AD. Meanwhile, the fact that localized neuronal death/loss and synaptic impairment occur in AD should also be considered. Neuronal regeneration, which does not occur normally in the mammalian central nervous system, can be promoted by neurotrophic factors （NTFs）. Evidence from clinical trials has shown that both Aβ clearance and NTFs are potentially effective in treating AD, thus a new approach combining Aβ clearance and administration of NTFs may be an effective therapeutic strategy.展开更多
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 cortic...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.展开更多
基金supported by the National Natural Science Foundation of China(30672450)the National Basic Research Development Program(973Program)of China(2011CB707500)
文摘There is no effective drug to treat Alzheimer＇s disease （AD）, a neurodegenerative disease affecting an estimated 30 million people around the world. Strongly supported by preclinical and clinical studies, amyloid-beta （Aβ） may be a target for developing drugs against AD. Meanwhile, the fact that localized neuronal death/loss and synaptic impairment occur in AD should also be considered. Neuronal regeneration, which does not occur normally in the mammalian central nervous system, can be promoted by neurotrophic factors （NTFs）. Evidence from clinical trials has shown that both Aβ clearance and NTFs are potentially effective in treating AD, thus a new approach combining Aβ clearance and administration of NTFs may be an effective therapeutic strategy.
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)
文摘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.
