檀木檀香亚种柠檬酸类物质通过调节脂多糖诱导的巨噬细胞的NF-κB信号通路,发挥抗炎作用。
Chukrasia tabularis limonoid plays anti-inflammatory role by regulating NF-κB signaling pathway in lipopolysaccharide-induced macrophages.
发表日期:2023
作者:
Jinhuang Shen, Fan Cao, Zhiyong Huang, Xinhua Ma, Nana Yang, Haitao Zhang, Yonghong Zhang, Zhiqiang Zhang
来源:
TROPICAL MEDICINE & INTERNATIONAL HEALTH
摘要:
金黄樟橼(Chukrasia tabularisis)是一种著名的热带树木,原产于中国东南部地区,具有抗炎和抗氧化活性,并含有大量的柠檬苷和三萜类物质。本研究的目的是研究金黄樟橼中柠檬苷对脂多糖(LPS)介导的RAW264.7细胞的潜在抗炎活性。通过生物活性引导法,找到具有较高抗炎活性的化学分馏物,并对其化学成分进行了研究。对活性提取物的植物化学研究结果表明,除了两种已知的柠檬苷(4-5)和11种三萜类三萜(6-16)之外,还分离得到了三种新型苯分枝内酯柠檬苷(1-3)。评估了这些分离化合物在LPS处理的巨噬细胞中一氧化氮(NO)的产生。柠檬苷2表现出显著的抗炎活性,IC50值为4.58μM。柠檬苷2显著抑制了巨噬细胞中NO、白细胞介素6和肿瘤坏死因子α的产生。柠檬苷2有效地阻断了信号传导和STAT和NF-κB激活剂的激活。这些结果表明,柠檬苷2通过抑制JAK2/STAT3、iNOS/eNOS和NF-κB信号通路以及调节炎性介质发挥抗炎作用。© 2023 申金黄等。
Chukrasia tabularisis, a well-known tropical tree native to southeastern China, has anti-inflammatory and antioxidant activities, and contains large amounts of limonoids and triterpenoids.The aim of this study was to investigate the potential anti-inflammatory activity of limonoids from C. tabularis on lipopolysaccharide (LPS)-mediated RAW264.7 cells.Using a bioassay-guided approach, the chemical fraction with high anti-inflammatory activity was found and its chemical constituents were investigated. Phytochemical studies on active extracts resulted in the separation of three novel phragmalin limonoids (1-3), together with two known limonoids (4-5) and 11 tirucallane triterpenes (6-16). The activity of these isolated compounds in the production of nitric oxide (NO) on LPS-reated macrophages was evaluated. Limonoid 2 indicated significant anti-inflammatory activities with IC50 value of 4.58 μM. Limonoid 2 notably inhibited the production of NO, interleukin- 6 and tumor necrosis factor-α on macrophage. Signal transduction and activation of STAT and NF-κB activators were effectively blocked by limonoid 2.These results indicate that limonoid 2 has an anti-inflammatory effect by the inhibiting JAK2/STAT3, iNOS/eNOS, and NF-κB signaling pathways and regulating inflammatory mediators.© 2023 Jinhuang Shen et al.