摘要
目的观察在缺氧条件下,Aβ干预人神经母细胞瘤细胞株(PAJU-ICAM-5细胞及PAJU-NEO细胞)后细胞株凋亡的情况,探讨缺氧环境中ICAM-5对Aβ神经毒性作用有无影响。方法将人神经母细胞瘤细胞分为常态组、Aβ干预组、缺氧组、缺氧+Aβ干预组。用倒置相差显微镜观察细胞形态的变化、MTT法观察细胞凋亡的情况。结果倒置相差显微镜下观察:PAJU-ICAM-5及PAJU-NEO细胞中缺氧组、Aβ组、缺氧并Aβ干预组较常态组细胞突起变短、减少,PAJU-ICAM-5细胞突起的长度较PAJU-NEO细胞的突起长。MTT染色:PAJU-ICAM-5细胞及PAJU-NEO细胞中缺氧组及Aβ组的细胞存活率较常态组降低(P<0.05),缺氧并Aβ干预组的细胞活性较常态组明显降低(P<0.01),缺氧组与Aβ组比较,其存活率无显著变化(P>0.05)。结论 Aβ42能引起PAJU细胞的凋亡,缺氧能促进其凋亡;ICAM-5可以减轻Aβ42的神经毒性作用。
Objective To observe the effect of Aβpeptide on PAJU-ICAM-5 cells and PAJU-NEO cells apoptosis under hypoxia condition and explore the effect of ICAM-5 on PAJU cells apoptosis by Aβ acting.Methods Cells were divided into 8 subgroups:①normal group:50 ml/L culturing PAJU-ICAM-5 and PAJU-NEO cells in CO2 box for 96 h;②Aβgroup:giving PAJU-ICAM-5 and PAJU-NEO cells 1.0 nmol/L aged Aβ42,then cultured for 96 h;③hypoxia group:culturing PAJU-ICAM-5 and PAJU-NEO cells in 1%~2% O2,5% CO2,93%N2 box for 96 h;④Aβ+ hypoxia group:giving PAJU-ICAM-5 and PAJU-NEO cells 1.0 nmol/L aged Aβ42,culturing them in 1%~2% O2,5% CO2,93%N2 box for 96 h.Cells were observed by microscope and MTT method.Results The number of PAJU-ICAM-5 and PAJU-NEO cells were decreased,and the dendrites of them became shortened compared with controlled ones under microscope.The activity of PAJU-ICAM-5 and PAJU-NEO cells was decreased also compared with controlled ones in MTT method test.Conclusions Aβ42 can cause PAJU cells apoptosis and hypoxia can enhance this procession.ICAM-5 can protect PAJU cells against the injury of Aβ.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2011年第19期3746-3748,共3页
Chinese Journal of Gerontology
基金
湖南省保健专项资金(No.B-2008-06)
湖南省自然科学基金项目(No.10JJ6051)