Wild radish (Raphanus sativus var. hortensis f. raphanistroides) root extract protects neuronal cells by inhibiting microglial activation

Abstract

AbstractExternal stimulus-induced activation of microglia plays an important role in the protection of neurons in the central nervous system; however, over-activation of microglia could cause neuronal damage, and it is implicated in the pathogenesis of neurodegenerative diseases. The aim of the present study was to investigate the effects of wild radish (Raphanus sativus var. hortensis f. raphanistroides) root extract (WRE) on microglial over-activation. Mouse microglia BV-2 cells and rat primary microglia were stimulated with lipopolysaccharide (LPS), treated with WRE, and analyzed for nitric oxide (NO) production, pro-inflammatory cytokine secretion, inducible NO synthase (iNOS) expression, and p38 kinase phosphorylation. Human neuroblastoma SH-SY5Y cells were treated with microglia-conditioned medium and analyzed for cell viability. Stimulation with LPS increased NO production and iNOS expression in BV-2 cells and primary microglia, but the treatment with WRE decreased both. Furthermore, WRE downregulated the mRNA expression and secretion of inflammatory cytokines interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α), and inhibited the phosphorylation of p38 in LPS-activated microglia. Treatment with the conditioned medium of LPS-induced BV-2 cells decreased the viability of SH-SY5Y cells, but the damaging effect was significantly alleviated in cells treated with the conditioned medium of LPS plus WRE-cultured microglia. This indicated that the WRE treatment of microglia could protect neuronal cells from microglial activation-induced neurotoxicity. WRE may be a potential food product to attenuate neuroinflammation via the inhibition of microglial over-activation, which can slow down the neurodegenerative processes in the brain.