it is important to continue efforts to discover new treatments

As shown in the following chart, 20 uM Abetinduced decrease in PC12 cell viability with time dependent manner. We also used the get a grip on peptide 20 uM Abetto establish the effect of 20 uM Abeton the cell viability As shown in the next BAM7 Bcl-2 inhibitor data, 20 uM Abethad no effect on PC12 cell viability. Hoechst 33258 staining also showed 10 uM Abetand 20 uM Abetcould induce PC12 cell apoptosis. How-ever, 10 uM Abetand 20 uM Abethad no influence on PC12 cell apoptosis. Ramifications of Epo on Abetinduced PC12 cell viability and cell apoptosis decided by MTT and Hoechst 33258 staining respectively We included 3 different concentrations of Epo to the serum deprived mediof PC12 cells 1 h prior to the 24 h 20 uM Abetexposure. As shown in the following data, different concentrations of Epo could effortlessly prevent loss of cell viability induced by 20 uM Abeta. Hoechst 33258 staining also showed Chromoblastomycosis 3 different levels of Epo could effectively prevent cell apoptosis induced by Abeta. Ramifications of Epo on Abetinduced PC12 cell apoptosis established by Western blotting Using Western blotting analysis, we discovered that the Abettreatment of PC12 cells could reduce the expression of Bcl 2 and increase the expression of Bax, Cleaved casapase 3, and Cleaved PARP. Three different Epo concentrtions may reduce 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 demonstrated an ability to activate the PI3KAkt signal transduction pathway, which regulates cell survival and proliferation. We treated 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 suggested that the PI3KAkt pathway was involved in buy NSC-66811 Abetinduced cell apoptosis, When the PI3K pathway was inhibited by LY294002 in PC12 cells, we found that the consequences of Epo on Abetinduced cell accidents were reduced. Debate Abetis the major element of SPs, which are consid ered to perform causal role in the development and pro gress of AD. The molecular mechanisms underlying Abetmediated neurotoxicity remain unclear. Recently, many in vitro and vivo studies have shown that Abetcan right induce neuronal death vithe mechanism of apoptosis. Epo is well known for its position as hematopoetic hormone. Epo binds to specific receptors within the human brain might be produced by astrocytes as well as neurons. Epo was proved to be capable of crossing the blood CSF barrier virecep tor mediated transfer and to behave as neuro trophic factor supporting the differentiation and regeneration of nerves. Their protective effect under conditions of neuronal injury was also reported. Consequently, we suggested that the Epo system in the CNS can act as an endogenous system for avoiding neuro-degenerative diseases such as AD.