ABSTRACT
In order to examine the effect of IGF-1 on neurogenesis after focal cerebral ischemia in young and olderrats.IGF-1 was applied by transventricular injection one day before operation of permanent middle cerebral artery occlusion(MCAO).Incontrast,the control groups were treated with vehicle. Methods: Bromodeoxyuridin (BrdU) was used as a marker of the proliferating cells,and PSA-NCAM as a marker of neural precursor cells,BrdU-labeled cells immunoreacted With MAP2 as a marker of differentiated neural precursor cells 28d after MCAO.Rats were administered With BrdU 6 days after MCAO.Immunohistochemistry was used to de-tect the expression of BrdU and PSA-NCAM immtmoreactivity in cortex and hippocampus 7 days and 28 days after MCAO.double im-munohistochemistry was used to detect the expression of MAP2 of BrdU.labeled cells 28d after MCAO.Results:The number of BrdU-labeled cells and PSA-NCAM positive cells increased 5.1 fold and 3.2 7d after 1GF-1 infusion in older rats.and 5.5 fold and 3.2 fold in young r ts.compared with vehicle.treated group(p>0.05).The residual rate of BrdU.labeled cells were 79.2%and 75.1% respectively inyoungandolderrats (p>0.05),incontraryt 077.1% and 52.3%(p<0.05)invehicle.treatedgroups 28d after MCAO.BrdU/MAP2 positive cells increased after IGF.1 infusion with more clear effect in young group(p<0.05),compared with vehicle.treated group.Conclu-sion:Our results indicated that IGF-1 pretreatment induced the neurogenesis,ameliorated the survival of post-proliferation cells in MCAO rats and induced neural precursor cells to differentiate into neuron.Our finding will be helpful to developing therapeutic applica-t-ion of IGF.1 after brain injury in older patients.
ABSTRACT
In order to examine the effect of IGF-1 on neurogenesis after focal cerebral ischemia in young and olderrats.IGF-1 was applied by transventricular injection one day before operation of permanent middle cerebral artery occlusion(MCAO).Incontrast,the control groups were treated with vehicle. Methods: Bromodeoxyuridin (BrdU) was used as a marker of the proliferating cells,and PSA-NCAM as a marker of neural precursor cells,BrdU-labeled cells immunoreacted With MAP2 as a marker of differentiated neural precursor cells 28d after MCAO.Rats were administered With BrdU 6 days after MCAO.Immunohistochemistry was used to de-tect the expression of BrdU and PSA-NCAM immtmoreactivity in cortex and hippocampus 7 days and 28 days after MCAO.double im-munohistochemistry was used to detect the expression of MAP2 of BrdU.labeled cells 28d after MCAO.Results:The number of BrdU-labeled cells and PSA-NCAM positive cells increased 5.1 fold and 3.2 7d after 1GF-1 infusion in older rats.and 5.5 fold and 3.2 fold in young r ts.compared with vehicle.treated group(p>0.05).The residual rate of BrdU.labeled cells were 79.2%and 75.1% respectively inyoungandolderrats (p>0.05),incontraryt 077.1% and 52.3%(p<0.05)invehicle.treatedgroups 28d after MCAO.BrdU/MAP2 positive cells increased after IGF.1 infusion with more clear effect in young group(p<0.05),compared with vehicle.treated group.Conclu-sion:Our results indicated that IGF-1 pretreatment induced the neurogenesis,ameliorated the survival of post-proliferation cells in MCAO rats and induced neural precursor cells to differentiate into neuron.Our finding will be helpful to developing therapeutic applica-t-ion of IGF.1 after brain injury in older patients.