Anti-inflammatory and anti-oxidative effects of Centella asiatica extract in lipopolysaccharide-stimulated BV2 microglial cells

Background: Neuroinflammation and oxidative stress mediated by microglial activation have been reported to play a critical role in the pathogenesis of neurodegenerative diseases. Therefore, inhibition of microglial activation using herbal medicine may be a potential candidate for the treatment of such diseases. Objective: The goal of this study was to investigate the anti-inflammatory and anti-oxidative effects of Centella asiatica extract (CA) on lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Methods: BV2 microglial cells were treated with LPS in the presence or absence of CA extract. The levels of nitric oxide (NO), tumor necrosis factor-α (TNF-α) and reactive oxygen species (ROS) was measured using Griess reagent assay, enzyme-linked immunosorbent assay (ELISA) assay and CM-H2DCFDA, respectively. The nuclear levels of nuclear factor kappa B (NF-kB) p65 were detected using immunofluorescence and ELISA assay. Results: CA treatment resulted in significant and concentration-dependently reduced the LPS-induced production of NO, TNF-α, and ROS compared to the untreated group. CA treatment exerted an anti-inflammatory effect by suppressing NF-kB p65 translocation and the activation of Akt and the extracellular-signal-regulated kinase 1/2 (ERK1/2) pathway in LPS-stimulated BV2 cells. Conclusion: Taken together, these results show that CA exerts antioxidative activity by suppressing ROS production and that it exerts anti-inflammatory activity by suppressing LPS-induced NO and TNF-α production in BV2 microglial cells. These effects may occur through inhibition of Akt and the ERK1/2-mediated NF-kB pathway. The results presented here, coupled with traditional therapeutic claims, suggest that CA may be beneficial for treating neurodegenerative diseases mediated by microglial cells.