Abstract
Purpose : To evaluate the protective effects of purple sweet potato (Ipomoea batatas Linn, Convolvulaceae) extract (IBE) in stimulated BV-2 microglial cells and its anti-oxidant properties. Methods : Cell viability assessment was performed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide (MTT) assay. Lipopolysaccharide (LPS) was used to activate BV-2 microglia. Nitric oxide (NO) levels were measured using Griess assay. Inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 expressional levels were measured by Western blot analysis. Tumor necrosis factor-alpha (TNF-α) production was evaluated by enzyme-linked immunosorbent assay (ELISA). Antioxidant properties were evaluated by 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) radical scavenging assay. Results : LPS-activated excessive release of NO in BV-2 cells was significantly inhibited by IBE (p<0.001 at 100 µg/mL). Increased production of inflammatory mediators such as iNOS, COX-2 and TNF-α (p < 0.01 and p < 0.001 at 100 and 200 µg/ml, respectively) was attenuated by IBE concentration-dependently. IBE also scavenged DPPH radicals in a dose-dependent manner (p < 0.05 at 10 ig/ml and p < 0.001 at 20 - 200 µg/ml). Conclusion : These results indicate that IBE attenuated neuroinflammatory responses in LPS-activated BV-2 microglia by inhibiting excessive production of pro-inflammatory mediators such as NO, iNOS, COX-2 and TNF-α. The anti-neuroinflammatory potential of IBE may be related to its strong antioxidant properties. Keywords : Ipomoea batatas, DPPH radicals, Anti-oxidant, Neuroinflammation, BV-2 microglia, Nitric oxide.
Highlights
Microglia cells are immune cells in the central nervous system (CNS) that able to produce several inflammatory mediators in response to stressors
Activated microglia and the released inflammatory mediators may lead to several neurodegenerative diseases including multiple sclerosis (MS), Parkinson’s disease (PD), Alzheimer’s disease (AD) and Huntington’s disease [2,3]
Treatment with I. batatas leaf (IBE) extract at indicated concentrations (10 μg/ml - 100 μg/ml) did not affect the overall cell viability nor did they exhibit any cytotoxicity on BV2 microglia cells
Summary
Microglia cells are immune cells in the central nervous system (CNS) that able to produce several inflammatory mediators in response to stressors. Activated microglia play a critical role in the neuroinflammatory processes by releasing toxic mediators including nitric oxide (NO), inducible NO synthase (iNOS), interleukins (IL), tumor necrosis factor-alpha (TNF-α), and free radicals [1]. Activated microglia and the released inflammatory mediators may lead to several neurodegenerative diseases including multiple sclerosis (MS), Parkinson’s disease (PD), Alzheimer’s disease (AD) and Huntington’s disease [2,3]. It is well known that microglia can be activated by lipopolysaccharide (LPS) and is recognized to be a useful in vitro tool for studying neuroinflammatory mechanisms [4]. Activated BV-2 microglia cells enhance the production of immune-related cytotoxic factors and pro-inflammatory cytokines [4,5]. The control of microglial activation has been suggested as a promising therapeutic target in combating neuroinflammatory-mediated neurodegenerative diseases
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