细胞间黏附分子5对Aβ诱发的PAJU细胞损伤的保护作用

Protective Effects of ICAM-5 on amyloid beta peptide induced neurites degeneration

目的探讨细胞间黏附分子5(ICAM-5)对β淀粉样蛋白(Aβ)诱导的PAJU细胞损伤的保护作用。方法采用较低浓度(0.5nM、0.8nM)Aβ42和Aβ35对转染人ICAM-5基因的PAJU-ICAM-5和转染空载体的PAJU-NEO细胞进行24h、48h和96h处理,使用相差显微镜观察和显微测量PAJU-ICAM-5和PAJU-NEO细胞突起长度,用免疫荧光显微镜观察突起末端改变。结果在细胞形态上,PAJU-ICAM-5细胞和PAJU-NEO细胞在经过Aβ处理后均出现了部分损伤表现,PAJU-ICAM-5细胞的损害较轻,形态较正常。显微测量结果显示,在分别经过0.5nM、0.8nM的Aβ35和Aβ42作用24h、48h时和96h时后,PAJU-ICAM-5细胞的突起长度均比PAJU-NEO细胞的突起长度长,两组细胞的突起长度比较均具有显著性差异(P<0.05,P<0.01)。免疫荧光结果显示,经过Aβ处理后,PAJU-NEO细胞的突起变钝、变短,末端成球状,而PAJU-ICAM-5细胞却很少见球状突起。结论ICAM-5可以促进PAJU细胞突起生长、能够减轻Aβ对PAJU细胞的形态损害,对PAJU细胞的突起具有保护作用。

Objective To investigate the effect of intercellular adhesion molecule-5 （ ICAM-5 ） on PAJU cells＇ injury induced by amy- loid beta peptide （Aβ42 and Aβ35 ）. Methods The human ICAM-5 gene transfected PAJU-ICAM-5 and empty vector transfected PAJU-NEO cells were used as neuronal models. Both PAJU-ICAM-5 and PAJU-NEO were treated with 0.5 nM and 0.8 nM of Aβ35 and Aβ42 respectively for 24 hrs, 48 hrs or 96 hrs. Contrast phase microscope was used to observe the changes of morphology and measure neurites length. Immunofiuorescence microscope was used to observe the changes in the neurites termination. Results Both PAJU- ICAM-5 and PAJU-NEO cells were partial injured after Aβ treatment. The PAJU-ICAM-5 cells had relatively normal morphous, with less severe injuries. The average neurites length of PAJU-ICAM-5 cells were significantly longer than that of PAJU-NEO cells 24, 48 and 96 hrs after 0. 5 nM and 0.8 nM of Aβ35 and Aβ42 treatment （ P 〈 0.05 or P 〈 0.01 ）. The immunofluorescence results showed that the neurites of PAJU-NEO cells were blunted and shorten and the neuritis termination became glomerated; but there were no similar changes in neurites of PAJU-ICAM-5 cells after Aβ treaetment. Conclusions ICAM-5 can induce outgrowth of PAJU cells and dimin- ish their morphologic impairments. It could protect PAJU-NEO cells from neurotoxicity induced by Aβ42 and Aβ35.