目的：中枢神经系统中的小胶质细胞调节神经炎症，导致广泛的神经病理改变。本研究调查了川陈皮素 (Nob) 衍生物 5-乙酰氧基-6,7,8,3',4'-五甲氧基黄酮 (5-Ac-Nob) 在脂多糖 (LPS) 激活的 BV2 小胶质细胞中的抗神经炎症特性材料与方法：通过MTT法、Griess法、流式细胞术、酶联免疫吸附法（ELISA）测定细胞活力、一氧化氮（NO）、活性氧（ROS）和LPS 刺激的 BV2 小胶质细胞中的促炎因子（白细胞介素 1β、IL-1β、白细胞介素 6、IL-6、肿瘤坏死因子 α、TNF-α 和前列腺素 E2、PGE2）。 Toll 样受体 4 (TLR4) 介导的骨髓分化初级反应基因 88 (MyD88)/核因子-κ B (NF-κB)、丝裂原激活蛋白激酶 (MAPK) 信号通路以及信号转导子和转录激活子 3 ( STAT3)通过蛋白质印迹法测量。在斑马鱼模型中证实了 NO 生成和促炎细胞因子 mRNA 的分析。结果：5-Ac-Nob 减少了细胞死亡、NO、ROS、诱导型一氧化氮合酶 (iNOS)、环氧合酶 2 (COX-2) 的水平）和 LPS 激活的 BV-2 小胶质细胞中的促炎因子。暴露于 5-Ac-Nob 后，TLR4 介导的 MyD88/NF-κB 和 MAPK 通路（p38、ERK 和 JNK）也受到抑制。此外，5-Ac-Nob 抑制 LPS 诱导的 BV-2 小胶质细胞中磷酸化 STAT3 蛋白的表达。此外，我们证实 5-Ac-Nob 可以减少斑马鱼模型中 LPS 诱导的 NO 生成和促炎细胞因子 mRNA。结论：我们的研究结果表明 5-Ac-Nob 通过抑制 TLR4 介导的信号通路来抑制神经炎症反应，并且统计3。这些发现的结果是，5-Ac-Nob 有潜力作为抗炎剂来对抗小胶质细胞介导的神经炎症性疾病。

Objective: Microglia in the central nervous system regulate neuroinflammation that leads to a wide range of neuropathological alterations. The present study investigated the anti-neuroinflammatory properties of nobiletin (Nob) derivative, 5-acetoxy-6,7,8,3',4'-pentamethoxyflavone (5-Ac-Nob), in lipopolysaccharide (LPS)-activated BV2 microglia.Materials and Methods: By using the MTT assay, Griess method, flow cytometry, and enzyme-linked immunosorbent assay (ELISA), we determined the cell viability, the levels of nitric oxide (NO), reactive oxygen species (ROS), and pro-inflammatory factors (interleukin 1 beta; IL-1β, interleukin 6; IL-6, tumor necrosis factor alpha; TNF-α and prostaglandin E2; PGE2) in LPS-stimulated BV2 microglia. Toll-like receptor 4 (TLR4)-mediated myeloid differentiation primary response gene 88 (MyD88)/nuclear factor-kappa B (NF-κB), mitogen-activated protein kinase (MAPK) signaling pathway and signal transducer and activator of transcription 3 (STAT3) were measured by western blotting. Analysis of NO generation and mRNA of pro-inflammatory cytokines was confirmed in the zebrafish model.Results: 5-Ac-Nob reduced cell death, the levels of NO, ROS, inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX-2) and pro-inflammatory factors in LPS-activated BV-2 microglial cells. TLR4-mediated MyD88/NF-κB and MAPK pathway (p38, ERK and JNK) after exposure to 5-Ac-Nob was also suppressed. Moreover, 5-Ac-Nob inhibited phosphorylated STAT3 proteins expression in LPS-induced BV-2 microglial cells. Furthermore, we confirmed that 5-Ac-Nob decreased LPS-induced NO generation and mRNA of pro-inflammatory cytokines in the zebrafish model.Conclusions: Our findings suggest that 5-Ac-Nob represses neuroinflammatory responses by inhibiting TLR4-mediated signaling pathway and STAT3. As a result of these findings, 5-Ac-Nob has potential as an anti-inflammatory agent against microglia-mediated neuroinflammatory disorders.