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神经生长因子(NGF)主要由神经胶质细胞产生,通过特异的靶细胞表面的神经生长因子受体介导产生生物学效应,与神经细胞的生长发育、分化和凋亡等密切相关。单纯疱疹病毒1型(HSV-1)作为一种嗜神经病毒,易造成神经细胞、神经胶质细胞凋亡或死亡。本实验以U251人神经胶质瘤细胞为研究对象,观察HSV-1感染致U251细胞凋亡的过程中NGF及其受体的变化情况。结果发现U251细胞是HSV-1的容许细胞;HSV-1感染致U251细胞凋亡过程中,NGF及其低亲和力受体p75NTR出现表达强度随时间先增强后减弱的趋势,而高亲和受体Tr-kA持续低表达。推测HSV-1感染致神经细胞凋亡中可能调控了神经营养因子的表达。
Nerve growth factor (NGF) is mainly produced by glial cells, through the specific target cell surface nerve growth factor receptor-mediated biological effects, and nerve cell growth and development, differentiation and apoptosis are closely related. Herpes simplex virus type 1 (HSV-1), a neurotropic virus, can easily cause neuronal or glial apoptosis or death. In this study, U251 human glioma cells as the object of study, HSV-1 infection induced apoptosis in U251 cells during NGF and its receptor changes. The results showed that U251 cells were the permissive cells for HSV-1. During the apoptosis of U251 cells induced by HSV-1, the expression intensity of NGF and its low-affinity receptor p75NTR tended to increase firstly and then decreased, while the high affinity receptor Tr-kA sustained low expression. Speculated that HSV-1 infection induced neuronal apoptosis may regulate the expression of neurotrophic factor.