Attenuation of Neuroinflammatory Responses in Lipopolysaccharide-Induced BV-2 Microglia by Suaeda asparagoides Miq. (Chenopodiaceae)

Purpose: To investigate the protective effect of Suaeda asparagoides (Chenopodiaceae) extract on neuroinflammatory responses induced by lipopolysaccharide (LPS) in BV-2 microglial cells and its antioxidant effects.Methods: Biochemical studies carried out include 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyl-tetrazolium bromide (MTT) assay and 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) assay for cell viability and radical scavenging activities, respectively. To evaluate the anti-neuroinflammatory effects of S. asparagoides (SAE) extract, LPS (1ìg/ml)-stimulated BV-2 microglial cells were used and pro-inflammatory mediators and cytokines such as nitric oxide (NO), inducible NO (iNOS), cyclooxygenase (COX)-2, tumor necrosisfactor-alpha (TNF-α) and nuclear factor-kappa B (NF-êB) were measured using Western blotting and enzyme-linked immunosorbent assay (ELISA).Results: LPS-stimulation of BV-2 cells increased the levels of NO (25.2 ± 2.15, p < 0.001) and proinflammatory mediators such as iNOS, COX-2 and TNF- α. However, treatment with SAE extract (20, 40 and 80 µg/ml) to LPS-stimulated BV-2 cells significantly inhibited the excessive release of NO (p < 0.05 at 20 µg/ml and p < 0.001 at 40 and 80 µg/ml, respectively) and suppressed the increased levels of iNOS, COX-2 and TNF-α. SAE also concentration dependently inhibited the NF-êB activation in LPSstimulatedBV-2 microglia. Further, SAE significantly and concentration-dependently (p < 0.001 at 20 - 200 µg/ml, respectively) scavenged DPPH radicals with IC50 of 36.33 ± 2.12 µg/ml.Conclusion: The results strongly suggest that SAE exhibits protective activity against LPS-stimulated neuroinflammatory responses. Mechanistic study reveals that SAE might by regulating NF-êB signaling. The antioxidant activity exhibited by SAE extract might also play a role in the plant’s significant antineuroinflammatory effect.Keywords: Suaeda asparagoides, Chenopodiaceae, Microglia, Lipopolysaccharide, Neuroinflammation, Cytokines, Antioxidan

Carum carvi Linn (Umbelliferae) Attenuates Lipopolysaccharide-Induced Neuroinflammatory Responses via Regulation of NF-κB Signaling in BV-2 Microglia

Purpose: To investigate the anti-neuroinflammatory properties of Carum carvi Linn. (CCE, Umbelliferae) aqueous extract in stimulated BV-2 microglial cells and explore its underlying mechanisms.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) levels were evaluated by Western blot analysis. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) production were evaluated by enzyme-linked immunosorbent assay (ELISA).Results: CCE alone did not exhibit any signs of cytotoxicity to BV-2 cells up to 200 μg/ml concentration. The LPS-activated excessive release of NO in BV-2 cells was significantly inhibited by CCE (p < 0.001 at 100 μg/mL). CCE also inhibited the production of inflammatory mediators such as iNOS, COX-2, IL-6 and TNF-α (p < 0.05, p < 0.01 and p < 0.001 at 25, 50 and 100 μg/mL, respectively). Further mechanistic study revealed that CCE acts by regulation of nuclear factor kappa-B (NF-κB) signaling pathway in LPS-stimulated BV-2 microglial cells.Conclusion: The results reveal that CCE exhibited its anti-neuroinflammatory effects via regulation of NF-κB signaling. This can be developed as a potential therapeutic target in ameliorating microgliamediated neuroinflammation.Keywords: Carum carvi, Anti-oxidant, Neuroinflammation, Microglia, Nitric oxide, Interleuki