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 (1μg/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 necrosis factor-alpha (TNF-α) and nuclear factor-kappa B (NF-κB) 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 pro-inflammatory 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-κB activation in LPS-stimulated BV-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-κB signaling. The antioxidant activity exhibited by SAE extract might also play a role in the plant’s significant anti-neuroinflammatory effect.