| Summary: | 碩士 === 國立臺灣海洋大學 === 生物科技研究所 === 92 === Neurodegeneration disease, for instance, Alzheimer’s Disease (AD) is the common cause of dementia among elderly people which affects at least 15 million persons throughout the world ( Reisberg. et al., 2003 ).
Excesssive production of nitric oxide ( NO ) in the central nervous system ( CNS ) mediated by activation of microglia has been implicated in neurotoxicity and neurodegeneration after stress such as ischemia, truma, and aging. We studied in LPS-stimulated BV-2 cells as a model of microglia activation and SNAP as a model of microglia apoptosis. Previous study had suggested that the inhibitory effect of olomoucine and roscovitine on BV-2 microglia activation and neurotoxic factor production is responsible for its neuroprotective action.
In the present study, we report the inhibitory effect of olomoucine on endotoxin / SNAP induced Rb、AP-1、 NF-κB transcription activity. From the transient transfection promoter activity assay, we found that olomoucine down regulate Rb transcription activity in SNAP induced Apoptosis pathway and also do the same way to Rb and NF-κB reporter genes in LPS induced Inflammation pathway. These results indicate that inactivation of NF-κB could be the major determinant for the suppression of iNOS promoter activity by olomoucine in BV2 microglia and AP-1 as the one of SNAP induced apoptosis by olomoucine in RBA-1.
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