Purpose: To investigate the suppressive effects of I. dentata on lipopolysaccharide (LPS)-induced neuroinflammatory responses in BV-2 microglia and its antioxidant effects.

Methods: Cell viability and free radical scavenging activities were performed using 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyl-tetrazolium bromide (MTT) and 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) assay, respectively. LPS (1μg/ml) was used to stimulate BV-2 microglia. Pro-inflammatory mediators such as nitric oxide (NO), inducible NO synthase (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.

Results: Treatment with I. dentata extract (ID-EA) significantly scavenged the DPPH radicals with IC50 value at 44.64 ± 2.64 μg/ml (p < 0.01 at 50 μg/ml). The increased levels of NO (23.32 ± 2.84 µM) and protein expressions of iNOS and COX-2 were inhibited by ID-EA extract in LPS-stimulated BV-2 cells. Increased pro-inflammatory cytokines such as TNF-α and IL-6 were also suppressed by ID-EA extract significantly (p < 0.001 at 80 µg/ml). Further, ID-EA extract blocked the expression of NF-κB activation in LPS-stimulated BV-2 cells.

Conclusion: Data from this study suggest that ID-EA extract possesses antioxidant effect and inhibits increased production of pro-inflammatory responses in LP5-stimulated BV-2 cells by suppressing NF-κB activation pathway. The significant inhibition of neuroinflammatory responses in stimulated microglial cells together with strong antioxidant activity may indicate that ID-EA can be developed as a therapeutic compound for treating neuroinflammatory diseases.