New Modes of GPCR Signalling

Akt Overexpression Opposes the Beta Amyloid Toxic Injuries to
HEK293/tau Cells
Yin Gang,Zhou xin-wen,Wang jian-zhi
Department of pathology and pathophysiology, the key laboratory of neurological
diseases of the ministry of education ,tongji medical college,huazhong university of
science and technology,wuhan 430030,china
Aim:To study the effect of a direct akt overexpression on Aβ-induced toxic injuries to
neuronal cells.. Methods:To evaluate the effect of Aβ-induced toxic injuries on
neuronal cells,we treated HEK293/tau neurons with several doses of Aβ for 24h.cells
were simultaneously transfected with several doses of a gene akt for 48h. CCK-8 KIT
assay the cell viability,and Reactive oxygen species assay kit assay the level of the level
of the Reactive oxygen species.the apoptosis was detected by flow cytometry.Results:
CCK-8 KIT assay showed that Aβ decreased neuronal cell viability in a
concentration-dependent manner and also that akt overexpression effectively prevented
Aβ-induced neuronal cell death. Aβ treatments increased ROS production in
HEK293/tau cells. Overexpression of Akt but not Akt mutant in the HEK293/tau cells
significantly attenuated Aβ induced ROS production and lipids peroxidation.
Furthermore, overexpression of Akt also attenuated Aβ-induced mitochondrial
dysfunction and apoptosis, and promoted cell survival in HEK293/tau cells.Conclusion:
the neurotoxic effect of Aβ can be partially prevented by akt overexpression.
Key Words: amyloid-beta;akt overexpression; toxic injury;oxidative stress
Author: Yin gang (1977-) was born in xiantao hubei,now I am study in Huazhong
University of Science and Technology for Ph.D, The direction of reseach is the
diagnosis and treatment of alzheimer’s disease. Email: 7706190@163.com, Tel:
13986672302