in contrast to other studies using different methodologies

the Abetrepresents the shortest fragment of Abeta, prepared in vivo by head proteases. BAM7 This peptide may be the practical domain of Abetrequired for neurotoxic influence, retaining the toxicity of the full length peptide. It is highly cytotoxic to neuronal cells and is widely used in both in vitro and in vivo experiments. In the pre sent research, we used Abetto see the toxic effect of Abetand the protecting effect of Epo. Abeta, 11 amino acid with reverse sequence of Abetwas used as get a grip on. We discovered that aggregated 20 uM Abetcould decrease cell viability over time depen dent manner, However, 20 uM Abethad no impact on PC12 cell viability. Hoechst 33258 staining showed while Abethad no effect on PC12 cell apoptosis Abetcan induce PC12 cell apoptosis. Epo can attenuate the reduced cell viability and enhanced cell apop tosis induced by Abeta. Apoptosis is tightly Metastasis controlled process involving changes in the expression of unique set of genes. Bcl 2 is key member of the anti apoptotic Bcl 2 family, which plays key role in regulating mitochondrial mediated apoptotic cell death. Over-expression of Bcl neuronal cells can be protected by 2 from insult. In contrast, Bax belongs to the professional emergency subfamily, which encourages apoptosis by translocating to the mito chondrial membrane and facilitating cytochrome c release. In the present study, we observed 20 uM Abetexposure could produce a growth of Bax expres sion and decrease Bcl 2 expression in serum deprived cultured PC12 cells, and these changes could be effectively attenuated by Epo. Caspases are category of cysteine proteases and are cri tical mediators NSC-66811 of cell apoptosis, which play an impor tant part in the process. As an executor caspase 3 acts, it may activate DNfragmenttion factor, which activate endonucleases to cleave nuclear DNA, and ultimately contributes to cell death. Activation of caspase 3 is apparently crucial function in delivery of the apoptotic cascade in CNS dis eases such as Downs syndrome and AD. In this study, we also discovered 20 uM Abetexposure could induce an increase of Cleaved caspase 3 phrase, and Epo could effectively attenuate these changes. Significant evidence indicates that caspase 3 is either partially or fully accountable for the proteolytic cleavage of several essential proteins, including PARP. PARP is contains around one of the total nuclear proteins and that nuclear DNbinding protein of 110 kDthat is constitutively expressed in eukaryotes. PARP is very important for cell viability, and cleavage of PARP facilitates mobile dis-assembly and serves as marker of cells undergoing apop tosis. In this study, we also discovered 20 uM Abetexposure could induce a growth of Cleaved PARP expression and Epo could successfully attenuate these changes using the same tendency since the expression of Cleaved caspase 3. Epo elicits its effects by binding to specific cell surface receptors.