CAJ | 학술논문

为探讨人类免疫缺陷病毒(HIV)gp120对体外培养的大鼠背根神经节(DRG)神经元的神经毒性作用,我们建立了胎鼠DRG分散培养和器官型培养的模型.以上分散培养和器官型培养的DRG,经不同浓度(250 pmol/L,1 nmol/L)的HIV gp120处理(2次/7 d).分散培养的DRG细胞行微管相关蛋白2(MAP2)免疫荧光染色,然后利用荧光显微镜观察神经元胞体和突起的变化情况.器官型培养的DRG在电子显微镜下观察其超微结构的改变.经HIV gp120处理的神经元突起的数目和长度的变化,HIV gp120处理组与对照组相比有显著性意义(P＜0.001),而神经元的直径则没有变化(P＞0.05).应用以上不同浓度的HIV gp120处理后,神经元的超微结构出现明显改变,线粒体嵴减少或消失,微管和神经丝之间出现了大量的高电子密度颗粒.以上结果表明,HIV gp120对培养的DRG神经元具有直接的神经毒性作用,其中以线粒体的改变较为敏感.
위탐토인류면역결함병독(HIV)gp120대체외배양적대서배근신경절(DRG)신경원적신경독성작용,아문건립료태서DRG분산배양화기관형배양적모형.이상분산배양화기관형배양적DRG,경불동농도(250 pmol/L,1 nmol/L)적HIV gp120처리(2차/7 d).분산배양적DRG세포행미관상관단백2(MAP2)면역형광염색,연후이용형광현미경관찰신경원포체화돌기적변화정황.기관형배양적DRG재전자현미경하관찰기초미결구적개변.경HIV gp120처리적신경원돌기적수목화장도적변화,HIV gp120처리조여대조조상비유현저성의의(P＜0.001),이신경원적직경칙몰유변화(P＞0.05).응용이상불동농도적HIV gp120처리후,신경원적초미결구출현명현개변,선립체척감소혹소실,미관화신경사지간출현료대량적고전자밀도과립.이상결과표명,HIV gp120대배양적DRG신경원구유직접적신경독성작용,기중이선립체적개변교위민감.
To investigate the neurotoxic effect of human immunodeficiency virus (HIV) gp120 on cultured dorsal root ganglion (DRG)neurons in vitro, dissociated and organotypic mouse embryo's DRG cell culture models were established. Both dissociated and organotypic DRG cultures were treated with HIV gp120 in different concentration (250 pmol/L and 1 nmol/L, respectively, 2 times/7 days). For dissociated DRG cultural cells, microtubule-associated protein 2 (MAP2) immunofluorescent labeling was processed for observing the changes of neuronal cell body and neurites. The change of the ultrastructure in the organotypic cultured DRG was observed by electron microscopy.The difference of the number and length of neurites between the control group and HIV gp120 treated groups were significant (P＜0.001),whereas there was no significant difference in the diameter of neurons between them (P＞0.05). The ultrastructural changes included the decrease or loss of cristae in mitochondria and accumulation of many high densed particles between the microtubules and the neurofilaments by using both the concentrations of HIV gp120 treatment. The present results indicate that HIV gp120 had a directly neurotoxic effect on the cultured DRG neurons, especially more sensitive to mitochondria.