Kim Byung-Chul, Choi Joung-Woo, Hong Hye-Young, Lee Sin-Ae, Hong Suntaek, Park Eun-Hee, Kim Seong-Jin, Lim Chang-Jin
Division of Life Sciences, Kangwon National University, Chuncheon 200-701, Korea.
J Ethnopharmacol. 2006 Jul 19;106(3):364-71. doi: 10.1016/j.jep.2006.01.009. Epub 2006 Feb 20.
This work aimed to elucidate the anti-inflammatory mechanism of the n-BuOH subfraction (PL) prepared from fruiting bodies of Phellinus linteus. PL induced heme oxygenase-1 (HO-1) of the RAW264.7 macrophages in concentration- and time-dependent manner. It suppressed induction of inducible nitric oxide synthase (iNOS) and subsequent production of nitric oxide (NO) through down-regulation of iNOS promoter activity in lipopolysaccharide (LPS)-stimulated macrophages. Zn(II) protoporphyrin IX (ZnPP), a specific inhibitor of HO-1, partly blocked suppression by PL on iNOS promoter activity and NO production, which were elevated in LPS-stimulated macrophages. LPS was able to enhance NO production via reactive oxygen species (ROS) generation, c-Jun NH(2)-terminal kinase (JNK) and c-Jun induction. ZnPP prevented PL from down-regulating ROS generation and JNK activation in LPS-stimulated macrophages. Taken together, PL shows its anti-inflammatory activity via mediation of HO-1 in an in vitro inflammation model.
本研究旨在阐明从桑黄子实体中制备的正丁醇亚组分（PL）的抗炎机制。PL以浓度和时间依赖性方式诱导RAW264.7巨噬细胞中的血红素加氧酶-1（HO-1）。它通过下调脂多糖（LPS）刺激的巨噬细胞中诱导型一氧化氮合酶（iNOS）启动子活性，抑制iNOS的诱导及随后一氧化氮（NO）的产生。HO-1的特异性抑制剂原卟啉锌IX（ZnPP）部分阻断了PL对LPS刺激的巨噬细胞中iNOS启动子活性和NO产生的抑制作用，而这两者在LPS刺激的巨噬细胞中均有所升高。LPS能够通过活性氧（ROS）生成、c-Jun氨基末端激酶（JNK）和c-Jun诱导来增强NO的产生。ZnPP阻止PL下调LPS刺激的巨噬细胞中的ROS生成和JNK激活。综上所述，在体外炎症模型中，PL通过HO-1介导发挥其抗炎活性。
