indicating the high pharmacological potency of natural compounds

As shown in the following chart, 20 uM Abetinduced reduction in PC12 cell viability with time dependent manner. We also used the control peptide 20 uM Abetto determine the effect of 20 uM Abeton the cell viability As shown in the following graph, 20 uM Abethad no effect on PC12 cell viability. Hoechst 33258 staining also showed 10 uM Abetand 20 uM Abetcould induce PC12 cell apoptosis. AZD3839 BACE inhibitor How ever, 10 uM Abetand 20 uM Abethad no effect on PC12 cell apoptosis. Effects of Epo on cell apoptosis and Abetinduced PC12 cell viability determined by MTT and Hoechst 33258 staining respectively We included 3 different levels of Epo to the serum deprived mediof PC12 cells 1 h before the 24 h 20 uM Abetexposure. Numerous levels of Epo might efficiently prevent decrease of cell viability induced by 20 uM Abeta, as shown in the following graph. Hoechst 33258 staining also showed 3 different concentrations of Epo can effectively prevent cell apoptosis induced by Abeta. Ramifications of Epo on Abetinduced PC12 cell apoptosis determined Inguinal canal by Western blotting Using Western blotting analysis, we found that the Abettreatment of PC12 cells could reduce the expression of Bcl 2 and raise the expression of Bax, Cleaved casapase 3, and Cleaved PARP. Three different Epo concentrtions could stop most of the above changes induced by Abeta. PI3KAkt involvement in the results of Epo on Abetinduced cell accidents Stimulation of EpoRs by Epo has previously been shown to activate the PI3KAkt signal transduction pathway, which regulates cell survival and growth. We addressed the cells with PI3K inhibitor LY294002 and found the LY294002 treatment caused slight increase in cell apoptosis in PC12 cells with or without Abettreatment This proposed that the PI3KAkt pathway was involved in STK 029746 Abetinduced cell apoptosis, When the PI3K pathway was inhibited by LY294002 in PC12 cells, we found that the results of Epo on Abetinduced cell accidents were declined. Conversation Abetis the main component of SPs, which are consid ered to play causal role in the development and pro gress of AD. The molecular mechanisms underlying Abetmediated neurotoxicity remain unclear. Recently, several in vivo and vitro studies demonstrate that Abetcan immediately induce neuronal death vithe mechanism of apoptosis. Epo is well regarded for its position as hematopoetic hormone. Epo binds to specific receptors contained in the human brain might be synthesized by astrocytes as well as neurons. Epo was shown to be capable of crossing the blood CSF barrier virecep tor mediated transfer and to act as neuro trophic factor promoting the differentiation and regeneration of neurons. Its protective effect under conditions of neuronal injury was also reported. Therefore, we suggested that the Epo system in the CNS could act as an endogenous system for avoiding neuro-degenerative disorders such as AD.