Aucubin protects against lipopolysaccharide-induced acute pulmonary injury through regulating Nrf2 and AMPK pathways

Publication date: October 2018Source: Biomedicine & Pharmacotherapy, Volume 106Author(s): Yan-Ling Qiu, Xiao-Ning Cheng, Feng Bai, Li-Yun Fang, Hui-Zhong Hu, Da-Qing SunAbstractAucubin (Ai), a natural compound isolated from plants, including Aucuba japonica and Eucommia ulmoides, shows significant anti-inflammatory and anti-oxidative bioactivities. Here, we attempted to explore the protect effects of Ai on LPS-induced acute lung injury (ALI). Our results indicated that Ai increased the survival rate and ameliorated pathogenic processes in lipopolysaccharide (LPS)-induced mice. However, nuclear factor erythroid 2-related factor 2 (Nrf2) deletion may impede protective effect of Ai. Additionally, Ai reduced oxidative stress by down-regulating malondialdehyde (MDA) and O2· activity, and enhancing Nrf2-targeted signals, including heme oxygenase-1 (HO-1) and quinone oxidoreductase-1 (NQO-1). Also, Ai inhibited pro-inflammatory cytokines and phosphorylated-nuclear factor-κB (NF-κB) expression in LPS-administrated mice. However, these protective effects of Ai were suppressed in Nrf2-knockout mice. Importantly, Nrf2-deficiency showed no effects on phosphorylated AMP-activated protein kinase (p-AMPK) expression in mice treated with LPS and Ai. Similarly, in LPS-induced macrophages, Ai reduced reactive oxygen species (ROS) generation, elevated NQO-1 and HO-1 expression. LPS-stimulated pro-inflammatory cytokines and p-NF-κB were reversed by Ai. Of note, we found that Ai-induced Nrf2 ...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research