Summary: | 碩士 === 慈濟大學 === 藥理暨毒理學研究所 === 95 === A significant component of neuropathological and degenerative disease is neuroinflammation in which microglia activation plays an important role. The activation induced over production of nitric oxide (NO) and reactive oxygen species (ROS), leading to neuronal damage or death. Granulocyte-colony stimulating factor (G-CSF), a neurotrophic factor that processes neuroprotective and anti-neuroinflammatory effect against several neurological disorders. Its protective effect on microglia or/and neurons which was unclear. Findings demonstrated that LPS did not affect cell viability of individually cultured BV-2 or Neuro-2a cells but suppressed that of the co-cultured cells, suggesting the suppressed cell viability due to production of cytotoxic agents by LPS-activated BV-2 cells. The suppressed cell viability and LPS-induced nitrite production was restored by G-CSF pretreatment. In addition, the present investigation for demonstrated that G-CSF pretreatment suppressed LPS-induced nitrite production and inducible NO synthase (iNOS) expression but not ROS production in BV-2 cells. In conclusion, G-CSF may protect BV-2 and Neuro-2a co-cultured through suppression of LPS-induced NO but not ROS produced by activated BV-2 microglia cells.
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