Key Laboratory of Chemical Biology of Ministry of Education, Department of Natural Product Chemistry, School of Pharmaceutical Sciences, Shandong University, Jinan 250012, China.
Int J Mol Sci. 2019 Jan 25;20(3):507. doi: 10.3390/ijms20030507.
Hemp seed (Fructus cannabis) is rich in lignanamides, and initial biological screening tests showed their potential anti-inflammatory and anti-oxidative capacity. This study investigated the possible effects and underlying mechanism of cannabisin F, a hempseed lignanamide, against inflammatory response and oxidative stress in lipopolysaccharide (LPS)-stimulated BV2 microglia cells. Cannabisin F suppressed the production and the mRNA levels of pro-inflammatory mediators such as interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) in a concentration-dependent manner in LPS-stimulated BV2 microglia cell. Furthermore, cannabisin F enhanced SIRT1 expression and blocked LPS-induced NF-κB (Nuclear factor kappa B) signaling pathway activation by inhibiting phosphorylation of IκBα (Inhibit proteins of nuclear factor kappaB) and NF-κB p65. And the SIRT1 inhibitor EX527 significantly inhibited the effect of cannabisin F on pro-inflammatory cytokines production, suggesting that the anti-inflammatory effects of cannabisin F are SIRT1-dependent. In addition, cannabisin F reduced the production of cellular reactive oxygen species (ROS) and promoted the expression of Nrf2 (Nuclear factor erythroid-2 related factor 2) and HO-1 (Heme Oxygenase-1), suggesting that the anti-oxidative effects of cannabisin F are related to Nrf2 signaling pathway. Collectively, these results suggest that the neuro-protection effect of cannabisin F against LPS-induced inflammatory response and oxidative stress in BV2 microglia cells involves the SIRT1/NF-κB and Nrf2 pathway.
麻籽（大麻籽）富含木脂素酰胺，初步的生物学筛选测试显示它们具有潜在的抗炎和抗氧化能力。本研究调查了大麻素 F（一种麻籽木脂素酰胺）对脂多糖（LPS）刺激的 BV2 小胶质细胞炎症反应和氧化应激的可能作用及其潜在机制。大麻素 F 以浓度依赖的方式抑制 LPS 刺激的 BV2 小胶质细胞中促炎介质白细胞介素 6（IL-6）和肿瘤坏死因子-α（TNF-α）的产生和 mRNA 水平。此外，大麻素 F 通过抑制 IκBα（核因子 kappa B 抑制蛋白）和 NF-κB p65 的磷酸化，增强 SIRT1 表达并阻断 LPS 诱导的 NF-κB（核因子 kappa B）信号通路激活。并且 SIRT1 抑制剂 EX527 显著抑制了大麻素 F 对促炎细胞因子产生的影响，表明大麻素 F 的抗炎作用是 SIRT1 依赖性的。此外，大麻素 F 减少细胞活性氧（ROS）的产生，并促进 Nrf2（核因子红细胞 2 相关因子 2）和 HO-1（血红素加氧酶-1）的表达，表明大麻素 F 的抗氧化作用与 Nrf2 信号通路有关。总的来说，这些结果表明，大麻素 F 对 LPS 诱导的 BV2 小胶质细胞炎症反应和氧化应激的神经保护作用涉及 SIRT1/NF-κB 和 Nrf2 途径。
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