Inhibition of Lipopolysaccharide-Stimulated Neuro- Inflammatory Kuntze in BV-2 Microglial Cell Mediators by Tetragonia tetragonoides (Pall)

TLDR: The results suggest that TKE can be explored as a potential therapeutic agent for regulating microglia-mediated neuroinflammatory responses observed in several neurodegenerative diseases.

Abstract: Purpose: To investigate the in vitro antioxidant and anti-neuroinflammatory effects of Tetragonia tetragonoides (Pall.) Kuntze extract (TKE) in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Methods: To evaluate the effects of TKE, LPS-stimulated BV microglia were used and the expression and production of inflammatory mediators, namely, nitric oxide (NO), inducible NO synthase (iNOS) and tumor necrosis alpha (TNF-α) were evaluated. Antioxidant activity of TKE was measured using 1, 1diphenyl-2-picryl-hydrazyl (DPPH) assay. Cell viabilities were estimated by 3-(4, 5-dimethylthiazol-2-yl)2, 5- diphenyl-tetrazolium bromide (MTT) assay. Results: TKE significantly suppressed LPS-induced production of NO (p < 0.001 at 20, 40, 80 and 100 μg/ml) and expression of iNOS in BV-2 cells. TKE also suppressed LPS-induced increase in TNF-α level (p < 0.001at 100 μg/ml) in BV-2 cells. In addition, DPPH-generated free radicals were inhibited by TKE in a concentration-dependent manner. Conclusion: The results suggest that TKE can be explored as a potential therapeutic agent for regulating microglia-mediated neuroinflammatory responses observed in several neurodegenerative diseases.