Abstract

Ent-kaur-15-en-17-al-18-oic acid (LL-3) was demonstrated that it can inhibit LPS-induced nitric oxide (NO) production and macrophage migration, maintain homeostasis of oxidative stress, including increased mitochondrial membrane potential (MMP), decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and maintenance of superoxide dismutase (SOD) and glutathione (GSH) activities and inhibit oxidative stress-induced P38 and nuclear factor κB (NF-κB) pathways to decrease inducible nitric oxide synthase (iNOS), cyclooxygense-2 (COX-2), and tumour necrosis factor (TNF)-α mRNA expressions without marked cytotoxicity. These findings revealed that LL-3 could serve as a candidate lead compound for further studying anti-inflammatory therapies.

摘要

Ent -kaur-15-en-17-al-18-oic acid (LL-3) 被证明可以抑制 LPS 诱导的一氧化氮 (NO) 产生和巨噬细胞迁移，维持氧化应激的稳态，包括增加线粒体膜电位 (MMP)，活性氧 (ROS) 和丙二醛 (MDA) 水平降低，维持超氧化物歧化酶 (SOD) 和谷胱甘肽 (GSH) 活性并抑制氧化应激诱导的 P38 和核因子 κB (NF-κB)减少诱导型一氧化氮合酶 (iNOS)、环氧合酶-2 (COX-2) 和肿瘤坏死因子 (TNF)-α mRNA 表达的途径，而没有明显的细胞毒性。这些发现表明，LL-3 可以作为进一步研究抗炎疗法的候选先导化合物。