Aim/Purpose of the study:Inhibition of microglial activation using phytochemicals may be a potential candidate for the prevention of neurodegenerative diseases caused by neuroinflammation and oxidative stress. The goal of this study was to investigate the protective role of Biochanin A on lipopolysaccharide (LPS)-stimulated BV2 microglial cells. BV2 microglial cells were treated with LPS in the presence and absence of Biochanin A. Materials and methods: For this aim, nitric oxide production, nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6, Prostaglandin E2 (PGE2), and reactive oxygen species (ROS) levels, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), myeloid differentiation factor-88 (MyD88), and toll like receptor-4 (TLR-4) protein expressions, Akt and ERK1/2 phosphorylation levels were measured. Results:Biochanin A pretreatment resulted in significant and concentration-dependently reduced the LPS-induced production of nitric oxide, NF-κB p65, TNF-α, IL-1β, IL-6, PGE2, and ROS compared to the untreated group. Biochanin A prophylaxis exerted an anti-inflammatory effect by suppressing iNOS, COX-2, MyD88, and TLR-4 protein expressions and Akt and ERK1/2 pathway activation. Conclusion:Taken together, these results show that Biochanin A exerts antioxidant and anti-inflammatory activities, thus may be beneficial for preventing neurodegenerative diseases mediated by microglial cells.

研究目的/目的：使用植物化学物质抑制小胶质细胞活化可能是预防由神经炎症和氧化应激引起的神经变性疾病的潜在候选药物。这项研究的目的是调查Biochanin A对脂多糖（LPS）刺激的B​​V2小胶质细胞的保护作用。在存在和缺乏Biochanin A的情况下，用LPS处理BV2小胶质细胞。材料和方法：为此目的，一氧化氮的产生，核因子κB（NF-κB），肿瘤坏死因子α（TNF-α），白介素1β（IL-1β），IL-6，前列腺素E2（PGE2）和反应性氧（ROS）水平，诱导型一氧化氮合酶（iNOS），环氧合酶2（COX-2），髓样分化因子88（MyD88）和收费样受体4（TLR-4）蛋白表达，Akt和ERK1测量了/ 2个磷酸化水平。结果：与未处理组相比，Biochanin A预处理可显着且浓度依赖性地降低LPS诱导的一氧化氮，NF-κBp65，TNF-α，IL-1β，IL-6，PGE2和ROS的产生。预防生物chanin通过抑制iNOS，COX-2，MyD88和TLR-4蛋白表达以及Akt和ERK1 / 2途径的激活发挥抗炎作用。结论：综上所述，Biochanin A具有抗氧化和抗炎作用，可能对预防小胶质细胞介导的神经退行性疾病有益。