Anti-Inflammatory and Anti-Oxidative Effects of Centella asiatica Extract in Lipopolysaccharide-Stimulated BV2 Microglial Cells

Anti-Inflammatory and Anti-Oxidative Effects of Centella asiatica Extract in Lipopolysaccharide-Stimulated BV2 Microglial Cells


English :

ABSTRACT
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.
Key words: Akt, BV2 microglia, Centella asiatica,
extracellular‑signal‑regulated kinase 1/2, nuclear factor kappa B