TY - JOUR
T1 - Erythropoietin prevents PC12 cells from beta-amyloid-induced apoptosis via PI3K/Akt pathway
AU - Zhi-Kun, Sun
AU - Hong-Qi, Yang
AU - Zhi-Quan, Wang
AU - Jing, Pan
AU - Zhen, Hong
AU - Sheng-Di, Chen
N1 - Funding Information:
This study was supported by grants from the State Key Basic Research Program (No.2010CB945200), Shanghai Key Discipline Program (No.S30202), Shanghai Natural Scientific Fund (No. 09JC1416402,09ZR1419100), Program for Outstanding Medical Academic Leader (No. LJ 06003), and Shanghai Jiao Tong University Medical and Engineering Joint Key Project (No. YG2010ZD102).
PY - 2012/2/29
Y1 - 2012/2/29
N2 - Background: Several studies indicated that Erythropoietin (Epo) may provide remarkable neuroprotection in some neurological diseases. It also showed the significant decrease of Epo immunoreactivity in the cerebral cortex and hippocampus in aged rats, suggesting the role of Epo in the pathogenesis of age-related neurodegenerative diseases such as AD.Methods: The protective effect of Epo was studied in differentiated PC12 cells treated with Abeta. The viability of the cells, the apoptosis of the cells and the level of Bax, Bcl-2, cleaved caspase-3 and cleaved PARP expression were detected by MTT, Hoechst 33258 staining and Western blotting respectively.Results: 20 μM Abeta (25-35) could induce a decreased viability and a increased apoptosis in PC12 cell in a time-dependent manner. However, 20 μM Abeta (35-25) had no effect on cell viability and apoptosis. Western blot analysis also showed that Abeta(25-35) treatment could decrease the expression of Bcl-2 (P < 0.05) and increase the expression of Bax (P < 0.05), Cleaved casapase-3 (P < 0.05), and Cleaved PARP (P < 0.05). The pretreatment of Epo could effectively reverse all the above changes induced by Abeta(25-35) (P < 0.05). Furthermore, the protective effect of Epo could be blocked by PI3K inhibitor LY294002 (P < 0.05).Conclusions: Epo prevented cell injuries in PC12 cells exposed to the Abeta(25-35) and this effect may depend on the PI3K/Akt pathway. Our study provided an important evidence for the potential application of Epo in the therapy of Alzheimer's disease.
AB - Background: Several studies indicated that Erythropoietin (Epo) may provide remarkable neuroprotection in some neurological diseases. It also showed the significant decrease of Epo immunoreactivity in the cerebral cortex and hippocampus in aged rats, suggesting the role of Epo in the pathogenesis of age-related neurodegenerative diseases such as AD.Methods: The protective effect of Epo was studied in differentiated PC12 cells treated with Abeta. The viability of the cells, the apoptosis of the cells and the level of Bax, Bcl-2, cleaved caspase-3 and cleaved PARP expression were detected by MTT, Hoechst 33258 staining and Western blotting respectively.Results: 20 μM Abeta (25-35) could induce a decreased viability and a increased apoptosis in PC12 cell in a time-dependent manner. However, 20 μM Abeta (35-25) had no effect on cell viability and apoptosis. Western blot analysis also showed that Abeta(25-35) treatment could decrease the expression of Bcl-2 (P < 0.05) and increase the expression of Bax (P < 0.05), Cleaved casapase-3 (P < 0.05), and Cleaved PARP (P < 0.05). The pretreatment of Epo could effectively reverse all the above changes induced by Abeta(25-35) (P < 0.05). Furthermore, the protective effect of Epo could be blocked by PI3K inhibitor LY294002 (P < 0.05).Conclusions: Epo prevented cell injuries in PC12 cells exposed to the Abeta(25-35) and this effect may depend on the PI3K/Akt pathway. Our study provided an important evidence for the potential application of Epo in the therapy of Alzheimer's disease.
KW - Alzheimer's disease
KW - Apoptosis
KW - Beta-amyloid peptide
KW - Erythropoietin
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U2 - 10.1186/2047-9158-1-7
DO - 10.1186/2047-9158-1-7
M3 - Article
C2 - 23211059
AN - SCOPUS:84883602573
SN - 2047-9158
VL - 1
JO - Translational Neurodegeneration
JF - Translational Neurodegeneration
M1 - 7
ER -