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Dynamic expression of nerve growth factor and its receptor TrkA after subarachnoid hemorrhage in rat brain

Delayed ischemic neurologic deficit after subarachnoid hemorrhage results from loss of neural cells. Nerve growth factor and its receptor TrkA may promote regeneration of neural cells, but their expression after subarachnoid hemorrhage remains unclear. In the present study, a rat model of subarachno...

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Detalles Bibliográficos
Autores principales: Song, Jin-ning, Liu, Zun-wei, Sui, Long, Zhang, Bin-fei, Zhao, Yong-lin, Ma, Xu-dong, Gu, Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5020827/
https://www.ncbi.nlm.nih.gov/pubmed/27651776
http://dx.doi.org/10.4103/1673-5374.189193
Descripción
Sumario:Delayed ischemic neurologic deficit after subarachnoid hemorrhage results from loss of neural cells. Nerve growth factor and its receptor TrkA may promote regeneration of neural cells, but their expression after subarachnoid hemorrhage remains unclear. In the present study, a rat model of subarachnoid hemorrhage was established using two injections of autologous blood into the cistern magna. Immunohisto-chemical staining suggested that the expression of nerve growth factor and TrkA in the cerebral cortex and brainstem increased at 6 hours, peaked at 12 hours and decreased 1 day after induction of subarachnoid hemorrhage, whereas the expression in the hippocampus increased at 6 hours, peaked on day 1, and decreased 3 days later. Compared with those for the rats in the sham and saline groups, neurobehavioral scores decreased significantly 12 hours and 3 days after subarachnoid hemorrhage (P < 0.05). These results suggest that the expression of nerve growth factor and its receptor TrkA is dynamically changed in the rat brain and may thus participate in neuronal survival and nerve regeneration after subarachnoid hemorrhage.