Aims: To show that acetate attenuates neuroinflammatory responses in activated microglia.
Background: Dietary acetate supplementation alleviates neuroglial activation in a rat model of
neuroinflammation induced by intraventricular administration of lipopolysaccharide (LPS). However, the
precise mechanism(s) underlying the anti-inflammatory effect of acetate is not fully understood.
Objective: To determine whether acetate has inhibitory effects on LPS-induced neuroinflammatory
responses in microglia.
Methods: We examined LPS-stimulated nitric oxide (NO) production in primary rat microglia and BV-2
cells. Protein expression of inducible NO synthase (iNOS) was determined by western blot analysis. The
intracellular generation of reactive oxygen species (ROS) and glutathione (GSH) were also evaluated.
Results: In primary microglia, acetate decreased LPS-stimulated NO production in a dose-dependent
manner, reaching significance at greater than 10 mM, and cell viability was not affected. Acetate suppressed
LPS-induced expression of iNOS protein concomitantly with the decrease in NO. The LPS-induced
increase in intracellular ROS production was attenuated by acetate. In addition, acetate prevented LPSinduced reduction of GSH. Notably, such suppressive effects of acetate on NO and ROS production were
not observed in BV-2 cells.
Conclusion: These findings suggest that acetate may alleviate neuroinflammatory responses by attenuating
NO and ROS production in primary microglia but not in BV-2 cells.
Other: All animals received humane care and the animal protocols used in this study were approved by the
Ethics Committees for Animal Experimentation.