A prenylated flavonoid, cudraflavanone B, is isolated from Cudrania tricuspidata. In this study, we investigated its anti-inflammatory and anti-neuroinflammatory effects in lipopolysaccharide (LPS)-induced RAW264.7 and BV2 cells. In our initial study of the anti-inflammatory effects of cudraflavanone B the production of nitric oxide and prostaglandin E2 was attenuated in LPS-stimulated RAW264.7 and BV2 cells. These inhibitory effects were related to the downregulation of inducible nitric oxide synthase and cyclooxygenase-2. In addition, cudraflavanone B suppressed the production of pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor-α in LPS-induced RAW264.7 and BV2 cells. Moreover, the evaluation of the molecular mechanisms underlying the anti-inflammatory effects of cudraflavanone B revealed that the compound attenuated the nuclear factor-kappa B signaling pathway in LPS-induced RAW264.7 and BV2 cells. In addition, cudraflavanone B inhibited the phosphorylation of extracellular signal-regulated kinase mitogen-activated protein kinase signaling pathways in these LPS-stimulated cells. Thus, cudraflavanone B suppressed nuclear factor-κB, and extracellular signal-regulated kinase mitogen-activated protein kinase mediated inflammatory pathways, demonstrating its potential in the treatment of neuroinflammatory conditions.

从Cudrania tricuspidata 中分离出异戊二烯化黄酮类化合物 cudraflavanone B. 在这项研究中，我们研究了其在脂多糖 (LPS) 诱导的 RAW264.7 和 BV2 细胞中的抗炎和抗神经炎症作用。在我们对铜黄酮 B 抗炎作用的初步研究中，LPS 刺激的 RAW264.7 和 BV2 细胞中一氧化氮和前列腺素 E2 的产生减弱。这些抑制作用与诱导型一氧化氮合酶和环氧合酶-2 的下调有关。此外，cudraflavanone B 抑制了 LPS 诱导的 RAW264.7 和 BV2 细胞中促炎细胞因子的产生，如白细胞介素-6 和肿瘤坏死因子-α。此外，对铜黄酮 B 抗炎作用的分子机制的评估表明，该化合物减弱了 LPS 诱导的 RAW264.7 和 BV2 细胞中的核因子-κB 信号通路。此外，cudraflavanone B 抑制这些 LPS 刺激细胞中细胞外信号调节激酶丝裂原活化蛋白激酶信号通路的磷酸化。因此，cudraflavanone B 抑制核因子-κB，细胞外信号调节激酶丝裂原活化蛋白激酶介导的炎症通路，证明其在治疗神经炎症方面的潜力。