Activation of extracellular signal-regulated kinase 1/2 has been demonstrated in acute brain ischemia. We hypothesized that activated extracellular signal-regulated kinase 1/2 can protect hippocampal neurons from inju...Activation of extracellular signal-regulated kinase 1/2 has been demonstrated in acute brain ischemia. We hypothesized that activated extracellular signal-regulated kinase 1/2 can protect hippocampal neurons from injury in a diabetic model after cerebral ischemia/reperfusion. In this study, transient whole-brain ischemia was induced by four-vessel occlusion in normal and diabetic rats, and extracellular signal-regulated kinase 1/2 inhibitor (U0126) was administered into diabetic rats 30 minutes before ischemia as a pretreatment. Results showed that the number of surviving neurons in the hippocampal CA1 region was reduced, extracellular signal-regulated kinase 1/2 phosphorylation and KuT0 activity were decreased, and pro-apoptotic Bax expression was upregulated after intervention using U0126. These findings demonstrate that inhibition of extracellular signal-regulated kinase 1/2 activity aggravated neuronal loss in the hippocampus in a diabetic rat after cerebral ischemia/reperfusion, further decreased DNA repairing ability and ac- celerated apoptosis in hippocampal neurons. Extracellular signal-regulated kinase 1/2 activation plays a neuroprotective role in hippocampal neurons in a diabetic rat after cerebral ischemia/ reperfusion.展开更多
Apolipoprotein E plays a crucial role in inhibiting chronic neurodegenerative processes. Howev-er, its impact on neurological function following diffuse brain injury is still unclear. This study was designed to evalua...Apolipoprotein E plays a crucial role in inhibiting chronic neurodegenerative processes. Howev-er, its impact on neurological function following diffuse brain injury is still unclear. This study was designed to evaluate the therapeutic effects and mechanisms of action of apolipoprotein E mimetic peptide on diffuse brain injury. Apolipoprotein E mimetic peptide was administered into the caudal vein of rats with diffuse brain injury before and after injury. We found that apo-lipoprotein E mimetic peptide signiifcantly decreased the number of apoptotic neurons, reduced extracellular signal-regulated kinase1/2 phosphorylation, down-regulated Bax and cytochrome c expression, decreased malondialdehyde content, and increased superoxide dismutase activity in a dose-dependent manner. These experimental ifndings demonstrate that apolipoprotein E mimetic peptide improves learning and memory function and protects against diffuse brain injury-induced apoptosis by inhibiting the extracellular signal-regulated kinase1/2-Bax mito-chondrial apoptotic pathway.展开更多
Investigations on adsorption behavior of triphenylene(TP)and subsequent graphene self-assembly on Cu(111)were carried out mainly by using scanning tunneling microscopy(STM).At monolayer coverage,TP molecules formed a ...Investigations on adsorption behavior of triphenylene(TP)and subsequent graphene self-assembly on Cu(111)were carried out mainly by using scanning tunneling microscopy(STM).At monolayer coverage,TP molecules formed a long-range ordered adsorption structure on Cu(111)with an uniform orientation.Graphene self-assembly on the Cu(111)substrate with TP molecules as precursor was achieved by annealing the sample,and a large-scale graphene overlayer was successfully captured after the sample annealing up to 1000 K.Three different Moirépatterns generated from relative rotational disorders between the graphene overlayer and the Cu(111)substrate were observed,one with 4°rotation between the graphene overlayer and the Cu(111)substrate with a periodicity of 2.93 nm,another with 7°rotation and 2.15 nm of the size of the Moirésupercell,and the third with 10°rotation with a periodicity of 1.35 nm.展开更多
基金supported by the Hebei Province Natural Science Program,No.H2012401007a grant from the foundation Key Project of Hebei Province Education Ministry,No.ZD2010106
文摘Activation of extracellular signal-regulated kinase 1/2 has been demonstrated in acute brain ischemia. We hypothesized that activated extracellular signal-regulated kinase 1/2 can protect hippocampal neurons from injury in a diabetic model after cerebral ischemia/reperfusion. In this study, transient whole-brain ischemia was induced by four-vessel occlusion in normal and diabetic rats, and extracellular signal-regulated kinase 1/2 inhibitor (U0126) was administered into diabetic rats 30 minutes before ischemia as a pretreatment. Results showed that the number of surviving neurons in the hippocampal CA1 region was reduced, extracellular signal-regulated kinase 1/2 phosphorylation and KuT0 activity were decreased, and pro-apoptotic Bax expression was upregulated after intervention using U0126. These findings demonstrate that inhibition of extracellular signal-regulated kinase 1/2 activity aggravated neuronal loss in the hippocampus in a diabetic rat after cerebral ischemia/reperfusion, further decreased DNA repairing ability and ac- celerated apoptosis in hippocampal neurons. Extracellular signal-regulated kinase 1/2 activation plays a neuroprotective role in hippocampal neurons in a diabetic rat after cerebral ischemia/ reperfusion.
基金supported by Scientific Research and Development Plan of Hebei Province,No.20276102DKey Project of Scientific Research in Universities of Hebei Province in China,No.ZD2010106
文摘Apolipoprotein E plays a crucial role in inhibiting chronic neurodegenerative processes. Howev-er, its impact on neurological function following diffuse brain injury is still unclear. This study was designed to evaluate the therapeutic effects and mechanisms of action of apolipoprotein E mimetic peptide on diffuse brain injury. Apolipoprotein E mimetic peptide was administered into the caudal vein of rats with diffuse brain injury before and after injury. We found that apo-lipoprotein E mimetic peptide signiifcantly decreased the number of apoptotic neurons, reduced extracellular signal-regulated kinase1/2 phosphorylation, down-regulated Bax and cytochrome c expression, decreased malondialdehyde content, and increased superoxide dismutase activity in a dose-dependent manner. These experimental ifndings demonstrate that apolipoprotein E mimetic peptide improves learning and memory function and protects against diffuse brain injury-induced apoptosis by inhibiting the extracellular signal-regulated kinase1/2-Bax mito-chondrial apoptotic pathway.
基金Project supported by the National Key Research and Development Program of China(Grant No.2017YFB0503100)the National Natural Science Foundation of China(Grant No.11790313).
文摘Investigations on adsorption behavior of triphenylene(TP)and subsequent graphene self-assembly on Cu(111)were carried out mainly by using scanning tunneling microscopy(STM).At monolayer coverage,TP molecules formed a long-range ordered adsorption structure on Cu(111)with an uniform orientation.Graphene self-assembly on the Cu(111)substrate with TP molecules as precursor was achieved by annealing the sample,and a large-scale graphene overlayer was successfully captured after the sample annealing up to 1000 K.Three different Moirépatterns generated from relative rotational disorders between the graphene overlayer and the Cu(111)substrate were observed,one with 4°rotation between the graphene overlayer and the Cu(111)substrate with a periodicity of 2.93 nm,another with 7°rotation and 2.15 nm of the size of the Moirésupercell,and the third with 10°rotation with a periodicity of 1.35 nm.