Bridelia ferruginea Produces Antineuroinflammatory Activity through Inhibition of Nuclear Factor-kappa B and p38 MAPK Signalling

Abstract EN

Bridelia ferruginea is commonly used in traditional African medicine (TAM) for treating various inflammatory conditions.

Extracts from the plant have been shown to exhibit anti-inflammatory property in a number of in vivo models.

In this study the influence of B.

ferruginea (BFE) on the production of PGE2, nitrite, and proinflammatory cytokines from LPS-stimulated BV-2 microglia was investigated.

The effects of BFE on cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expressions were evaluated in LPS-activated rat primary microglia.

The roles of NF-κB and MAPK signalling in the actions of BFE were also investigated.

BFE (25–200 μg) inhibited the production of PGE2, nitrite, tumour necrosis factor-α (TNFα), and interleukin-6 (IL-6) as well as COX-2 and iNOS protein expressions in LPS-activated microglial cells.

Further studies to elucidate the mechanism of anti-inflammatory action of BFE revealed interference with nuclear translocation of NF-κBp65 through mechanisms involving inhibition of IκB degradation.

BFE prevented phosphorylation of p38, but not p42/44 or JNK MAPK.

It is suggested that Bridelia ferruginea produces anti-inflammatory action through mechanisms involving p38 MAPK and NF-κB signalling.