Abstract
Purpose: To evaluate the anti-oxidant and anti-neuroinflammatory effects of the Sargassum thunbergii extract (Mertens ex Roth) Kuntze (STE) in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells in vitro.Methods: STE antioxidative activity was evaluated with an Electron Spin Resonance (ESR)spectrometer, which measured 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) radical scavenging activity. Cell viabilities were estimated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assays. LPS-stimulated BV-2 microglia were used to study the expression and production of inflammatory mediators, such as nitric oxide (NO), inducible NO synthase (iNOS) and tumor necrosis alpha (TNF-α).Results: LPS treatment, following STE pretreatment, decreased NO production by 13 ~ 65% in a dosedependent manner (p < 0.001 at 20, 40, 80 and 100 μg/mL), and was associated with the downregulation of inducible nitric oxide synthase (iNOS) expression. STE also attenuated the TNF-α soluble protein by 16 ~ 47% (p < 0.01at 20, 40 and 80 μg/mL) in activated murine microglia. Furthermore, the DPPH-generated free radicals were inhibited by STE concentration-dependently.Conclusion: STE has therapeutic potential in the prevention or treatment of neurodegenerative and oxidative stress-related disorders.Keywords: Sargassum thunbergii, Neurodegenerative diseases, Anti-inflammatory, Microglial cells, Inducible nitric oxide synthase (iNOS), Tumor necrosis factor (TNF)-α
Highlights
Microglia, as immune cells of the central nervous system (CNS), produce a variety of inflammatory mediators in response to immunological stressors, and play a critical role in neuroinflammatory processes [1]
Sargassum thunbergii (STE) treatment did not result in cytotoxic overproduction of nitric oxide (NO) in BV-2 microglial cells treated for 24 h at concentrations up to 200 μg/mL
LPS treatment resulted in excessive production of NO
Summary
As immune cells of the central nervous system (CNS), produce a variety of inflammatory mediators in response to immunological stressors, and play a critical role in neuroinflammatory processes [1]. Upon activation by exposure to free radicals and lipopolysaccharides (LPS) [2], microglia secrete various bioactive molecules such as nitric oxide (NO), inducible NO synthase (iNOS), interleukins (IL) and tumor necrosis factor (TNF)-α [3]. Overproduction of these inflammatory mediators can cause a number of severe neuro-degenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), and Huntington’s disease [4,5]. LPS has been proven to induce microglial activation in response to Gramnegative bacterial infections [6] These prior experiments indicate that LPS-induced stimulation of microglia may be an potent mechanism to study in vitro. Studies have shown that antioxidant and anti-inflammatory agents may inhibit microglial activation, and protect neurons from cell death, a prominent symptom of various neurodegenerative disorders [6,7]
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