Overexpression of synuclein cytotoxicity and stimulation of the damaged.docVIP

 PAGE \* MERGEFORMAT 15 Overexpression of synuclein cytotoxicity and stimulation of the damaged Of: Jin Jin Yuan Yu and Bo Sun Jiandong Chen Naihong [Abstract] Objective To construct @ synuclein over-expression cell model and studied the expression @ synuclein cytotoxicity and molecular mechanism for Parkinson’s disease revealed (PD pathogenesis and may find potential targets for drugs to provide the basis. Methods fat plasmid transfection and overexpression @ synuclein stable Clones, MTT method, PI staining, fluorescence microscopy for the detection of over-expression @ synuclein on cell activity and differentiation, withdrawal of serum and MPP + injury, luciferase reporter gene detection and Western blot used to study the overexpression of NF B @ synuclein and related proteins signaling pathway. The results @ synuclein over-expression phenotype of cell differentiation had no effect, but DA can significantly reduce cell viability, and significantly increased withdrawal of serum injury and MPP + toxicity on cells injury. overexpression @ synuclein could significantly increase MPP + on NF B transcriptional activation of the inhibitory effect, the mechanism may be related to inhibition of IB @ the phosphorylation. conclusion is based on genetic background and environmental factors combination of PD research model to better fit the pathological process more scientific and reasonable. NF B signaling pathway may inhibit the activity of another new mechanism for the pathogenesis of PD for the pathway proteins may be PD-depth study of the treatment new drug development research. [Keywords:] Parkinson’s disease, @ synuclein, cell toxicity, MPP +, NF B Epidemiological survey of Parkinson disease (PD has become the world’s second largest after Alzheimer’s disease central nervous system degenerative diseases, but its etiology and pathogenesis is unclear. @ Synuclein is the first found in PD-related genes, the mutants (A53T, A30P, E46K was shown to the pathogen