Ethanol extract of Cnidium officinale exhibits anti-inflammatory effects in BV2 microglial cells by suppressing NF-κB nuclear translocation and the activation of the PI3K/Akt signaling pathway.

ABSTRACT

Chronic microglial activation endangers neuronal survival through the release of various toxic pro-inflammatory molecules; thus, negative regulators of microglial activation have been identified as potential therapeutic candidates for several neurological diseases. In this study, we investigated the inhibitory effects of an ethanol extract of Cnidium officinale rhizomes (EECO), which has been used as a herbal drug in Oriental medicine, on the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators, such as nitric oxide (NO) and prostaglandin E2 (PGE2), as well as that of pro-inflammatory cytokines in BV2 microglia cells. EECO significantly inhibited the excess production of NO and PGE2 in LPS-stimulated BV2 microglia cells. It also attenuated the expression of inducible NO synthase, cyclooxygenase-2, as well as that of pro-inflammatory cytokines, such as interleukin-1ß and tumor necrosis factor-α. Moreover, EECO exhibited anti-inflammatory properties by suppressing nuclear factor-κB (NF-κB) translocation and the activation of the phosphoinositide 3-kinase/Akt pathway in LPS-stimulated BV2 cells. These results indicate that EECO exerts anti-inflammatory effects in LPS-stimulated BV2 microglial cells by inhibiting pro-inflammatory mediators and cytokine production by blocking the NF-κB pathway. These findings suggest that EECO has substantial therapeutic potential for the treatment of neurodegenerative diseases accompanied by microglial activation.