Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/31641
Title: Role of Dexamethasone on NOX-2 (gp91 phox) - Dependent Production of reactive oxygen species in activated BV-2 microglia
Authors: HUO YINGQIAN
Keywords: microglia, Nox-2, dexamethasone, ROS, oxidative stress, MAPK
Issue Date: 10-Aug-2011
Source: HUO YINGQIAN (2011-08-10). Role of Dexamethasone on NOX-2 (gp91 phox) - Dependent Production of reactive oxygen species in activated BV-2 microglia. ScholarBank@NUS Repository.
Abstract: Nox-2 (also known as gp91phox), a subunit component of NADPH oxidases, generates reactive oxygen species (ROS). Nox-dependent ROS generation and nitric oxide (NO) release by microglia have been implicated in a variety of diseases in the central nervous system. Dexamethasone (Dex) has been shown to suppress the ROS production, NO release and inflammatory reaction of activated microglial cells. However, the underlying mechanisms remained unclear. The present study showed that the increased ROS production and NO release in activated BV-2 microglial cells by LPS were associated with increased expression of gp91phox and iNOS. Dex suppressed the upregulation of gp91phox and iNOS, as well as the subsequent ROS production and NO synthesis in activated BV-2 cells. This inhibition caused by Dex appears to be mediated by upregulation of MAPK phosphatase-1 (MKP-1) which antagonizes the activity of mitogen-activated protein kinases (MAPKs), since the overexpression of MKP-1 or inhibition of MAPKs (by specific inhibitors of JNK and p38 MAPKs), were found to downregulate the expression of gp91phox and iNOS and to inhibit the synthesis of ROS and NO in activated BV-2 cells. Moreover, Dex was unable to suppress the LPS-induced synthesis of ROS and NO in BV-2 cells transfected with MKP-1 siRNA. On the other hand, knockdown of gp91phox in BV-2 cells suppressed the LPS-induced ROS production and NO release. In conclusion, it is suggested that downregulation of gp91phox and overexpression of MKP-1 that regulate ROS and NO may form the potential therapeutic strategy for the treatment of neuroinflammation in neurodegenerative diseases.
URI: http://scholarbank.nus.edu.sg/handle/10635/31641
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