The Role Of C.chinensis Extract Protecting PC12 Cell From Apoptosis Induced By 1-methyl-4-phenylpyridinium

The apoptotic model of Parkinson's disease in vitro was made by 1-methyl-4-phenylpyridinium ion (MPP+) in PC12 cells. At the early stage of MPP+ treatment, expression of Bcl-2 declined and expression of p53 and Bax increased. It suggested that MPP+-induced apoptosis maybe involved in mitochondria-dependent signal transduction pathway.Powered seeds of Cuscuta Chinensis Lam were macerated with methanol at room temperatures and the extract was evaporated under reduced pressure to afford brown syrup. According to the polarity, the residue was isolated with petroleum ether, chloroform, ethyl acetate, and n-BuOH respectively. Combined with cell viability analysis, the ethyl acetate fraction was confirmed as neuroprotective component and subjected to gel and polyamide column chromatography to provide an extract fraction.1-methyl-4-phenylpyridinium ion (MPP+) induced apoptosis in PC 12 cells was used as a model to screen the neuroprptective components from C. Chinensis. Pretreated PC12 cells with C. chinensis extracts for 30min prior to MPP+, PC 12 cells were then incubated for 48h at room temperature. The apoptosis rate declined to 6.3±0.16%. C. chinensis extracts suppressed appearance of morphological changes and apoptotic bodies. The mechanism maybe involved in C. Chinensis extracts not only suppressed the up-regulation of Bcl-2, Bax and the release of mitochondrial cytochrome c to cytosol, but also attenuated caspase-3 activation, and eventually protected against MPP+-induced apoptosis.