Prevention and treatment of AD by over-expression of neuroglobin via ac-tivating PI3K/Akt signaling pathway
10.3969/j.issn.1000-4718.2014.12.009
- VernacularTitle:过表达脑红蛋白通过激活PI3K／Akt信号通路防治AD的体外研究
- Author:
Jun YANG
;
Songyang DAI
;
Yue XIANG
;
Xiong ZHANG
- Publication Type:Journal Article
- Keywords:
Neuroglobin;
SH-SY5Y cells;
Apoptosis;
Caspase-3/9;
PI3K/Akt signaling pathway
- From:
Chinese Journal of Pathophysiology
2014;(12):2166-2171
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To study the neuroprotective roles of neuroglobin (NGB) over-expression in the SH-SY5Y cells transfected with pAPPswe.METHODS:The plasmid pEGFP-NGB was successfully constructed and transfected into the SH-SY5Y cells, which were pretreated with pAPPswe.MTT assay was applied to detect the effect of NGB over-expres-sion on the cell survival rates.JC-1 staining was used to detect the level of mitochondrial transmembrane potential.The cell apoptosis was analyzed by flow cytometry.The effects of NGB over-expression on the protein level of p-Akt, Akt and caspase-3/9 were determined by Western blotting.The generation of Aβ42 in the cells was measured by ELISA.RE-SULTS:The cell survival rate was remarkably increased after transfection with NGB compared with control group and emp-ty plasmid group (P<0.05).The over-expression of NGB significantly inhibited the decrease in mitochondrial membrane potential induced by pAPPswe.The over-expression of NGB inhibited the apoptosis of the cells.Furthermore, over-expres-sion of NGB not only inhibited the expression of caspase-3 and caspase-9, but also induced the production of p-Akt, which was prevented by LY294002, an inhibitor of PI3K/Akt.The generation of Aβ42 was inhibited in the cells with the over-ex-pression of NGB.CONCLUSION: Over-expression of NGB significantly inhibits the SH-SY5Y cell injuries induced by pAPPswe and inhibits the expression of caspase-3/9, which is tightly related with cell apoptosis.Furthermore, the neuro-protective roles of NGB may be via activating PI3K/Akt signaling pathway.
