Piperine attenuates lipopolysaccharide (LPS)-induced inflammatory responses in BV2 microglia

- Piperine significantly inhibited LPS-induced TNF-α, IL-6, IL-1β, and PGE2 production in BV2 cells.
- Piperine dose-dependently inhibited LPS-induced NF-κB activation.
- Piperine was found to amplify the expression of Nrf2 and HO-1 up-regulated by LPS.
- The inhibition of inflammatory mediators by piperine can be reversed by transfection with Nrf2 siRNA.

Piperine, the chief alkaloid isolated from Piper nigrum, has been known to have anti-inflammatory effect. However, the effects of piperine on neuroinflammation have not been reported. In the present study, we evaluated the effects of piperine on neuroinflammation in BV2 microglia and investigated the molecular mechanism. The results showed that piperine significantly inhibited LPS-induced TNF-α, IL-6, IL-1β, and PGE2 production in BV2 cells. Western blot analysis showed that piperine dose-dependently inhibited LPS-induced NF-κB activation. Furthermore, piperine was found to amplify the expression of Nrf2 and HO-1 up-regulated by LPS. In addition, the inhibition of inflammatory mediators by piperine can be reversed by transfection with Nrf2 siRNA. In conclusion, piperine inhibited LPS-induced inflammatory response by activating Nrf2 signaling pathway. These results indicated that piperine may be a promising agent for the treatment of neurodegenerative diseases.