Acacetin is a flavonoid compound commonly present in several plants

20 uM Abetinduced reduction AZD3514 1240299-33-5 in PC12 cell viability in time dependent manner, as shown in the next graph. We also used the control peptide 20 uM Abetto establish the effect of 20 uM Abeton the cell viability As shown in the next 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. How ever, 10 uM Abetand 20 uM Abethad no effect on PC12 cell apoptosis. Effects of Epo on Abetinduced PC12 cell viability and cell apoptosis determined by Hoechst and MTT 33258 staining respectively We included 3 different concentrations of Epo in to the serum deprived mediof PC12 cells 1 h before the 24 h 20 uM Abetexposure. Various concentrations of Epo can effectively prevent loss of cell viability induced by 20 uM Abeta, as shown in the next data. Hoechst 33258 staining also showed 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 found that the Abettreatment of PC12 cells could reduce the expression of Bcl 2 and increase the Papillary thyroid cancer expression of Bax, Cleaved casapase 3, and Cleaved PARP. Three different Epo concentrtions could prevent most of the above improvements induced by Abeta. PI3KAkt participation in the consequences of Epo on Abetinduced cell accidents Stimulation of EpoRs by Epo has previously been proven to activate the PI3KAkt signal transduction pathway, which regulates cell survival and proliferation. 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 suggested that the PI3KAkt Marimastat MMP inhibitor pathway was involved in Abetinduced cell apoptosis, Once the PI3K pathway was inhibited by LY294002 in PC12 cells, we found that the results of Epo on Abetinduced cell accidents were reduced. Talk Abetis the main component 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, several in vitro and vivo studies demonstrate that Abetcan directly induce neuronal death vithe mechanism of apoptosis. Epo is widely-known for its role as hematopoetic hormone. Epo binds to specific receptors contained in the mind might be produced by neurons as well as astrocytes. 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. Its protective impact under conditions of neuronal damage was also reported. Therefore, we proposed the Epo system in the CNS can act as an endogenous system for avoiding neuro-degenerative disorders such as AD.