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.
