The increased production of Inducible Nitric Oxide Synthase (iNOS), one of the pathogenesis components of Alzheimer's disease and other neurodegenerative diseases, could be detected as one of endpoints in the oxidative-stress responses caused by the activation of primary microglia. Our aim was to explore the anti-oxidative effect of Astaxanthin (AST) on the primary microglia, derived from neonatal rats of Sprague Dawley(SD), mediated by Lipopolysaccharide (LPS).

First, primary microglia were isolated from primary mixed glia by Shake-off method, and stimulated by LPS. The primary microglia were identified through immunofluorescence while iNOS was measured by Western Blotting analysis. Secondly, this model was used to preliminarily explore the action of AST in the activated primary microglia induced by LPS.

Primary microglial cultures were confirmed using a specific CD11b antibody. iNOS was upregulated in the cells induced by LPS. The upregulation of iNOS was significantly different to that in the control (P<0.05), which suggested that the activated microglial model with oxidative stress be successfully established. Furthermore, 12.5, 25 or 50μg/ml of AST were pre-treated to the microglia for 24h before the application of LPS, which led to iNOS down-regulation at 12h, 24h or 36h, and the significant difference in the latter by comparing to that in LPS alone (P<0.05).

LPS led to the oxidative stress like iNOS upregulation in rat primary microglia. AST could down-regulated the oxidative stress such as iNOS in the microglia induced by LPS. This study suggested that AST can be with an antioxidative effect on the microglial activation in Alzheimer's disease and other neurodegenerative diseases. It may potentially be a valuable drug candidate in the clinics.