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Year : 2019  |  Volume : 15  |  Issue : 60  |  Page : 140-146

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

1 Department of Pre-Clinical, Faculty of Medicine, Mahasarakham University, Maha Sarakham, Bangkok, Thailand
2 Department of Anatomy, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand

Correspondence Address:
Nootchanat Mairuae
Faculty of Medicine, Mahasarakham University, Maha Sarakham 44000
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_197_18

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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. Abbreviations used: AD: Alzheimer's disease; ALS: Amyotrophic lateral sclerosis; CA: Centella asiatica; DMSO: Dimethyl sulfoxide; DMEM: Dulbecco's modified Eagle's medium; ECL: Enhanced chemiluminescence; ELISA: Enzyme-Linked immunosorbent assay; ERK1/2: Extracellular-signal-regulated kinase 1/2; FBS: Fetal bovine serum; LPS: Lipopolysaccharide; MS: Multiple sclerosis; MSU: Mahasarakham University; NF-kB: Nuclear factor kappa B; NO: Nitric oxide; PD: Parkinson's disease; ROS: Reactive oxygen species; SD: Standard deviation; TNF-α: Tumor necrosis factor-α.

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