External 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.

中文翻译：

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野生萝卜（萝卜变种菠菜F。raphanistroides）根提取物通过抑制小胶质细胞活化保护神经元细胞

外部刺激引起的小胶质细胞活化在中枢神经系统神经元保护中起着重要作用。然而，小胶质细胞的过度激活可能导致神经元损伤，这与神经退行性疾病的发病机制有关。本研究的目的是研究野生萝卜（Raphanus sativus var。hortensis f。raphanistroides）根提取物（WRE）对小胶质细胞过度活化的影响。用脂多糖（LPS）刺激小鼠小胶质细胞BV-2细胞和大鼠原发性小胶质细胞，用WRE处理，并分析一氧化氮（NO）的产生，促炎性细胞因子的分泌，诱导型一氧化氮合酶（iNOS）的表达和p38激酶的磷酸化。用小胶质细胞条件培养基处理人神经母细胞瘤SH-SY5Y细胞，并分析其细胞活力。用LPS刺激可增加BV-2细胞和原发性小胶质细胞的NO产生和iNOS表达，但用WRE处理均能降低。此外，WRE下调了炎症细胞因子白介素-1β（IL-1β）和肿瘤坏死因子α（TNF-α）的mRNA表达和分泌，并抑制了LPS激活的小胶质细胞中p38的磷酸化。用LPS诱导的BV-2细胞的条件培养基处理降低了SH-SY5Y细胞的活力，但是在用LPS和WRE培养的小胶质细胞的条件培养基处理的细胞中，损伤作用显着减轻。这表明WRE治疗的小胶质细胞可以保护神经元细胞免受小胶质细胞激活引起的神经毒性。WRE可能是通过抑制小胶质细胞过度激活而减轻神经炎症的潜在食品，