Emodin inhibits LPS-induced inflammatory response by activating PPAR-γ in mouse mammary epithelial cells

Emodin, an anthraquinone derivative isolated from the rhizomes of Rheum palmatum, has been reported to have a protective effect against lipopolysaccharide (LPS)-induced mastitis. However, the underlying molecular mechanisms are not well understood. The aim of this study was to investigate the molecular mechanisms of emodin in modifying lipopolysaccharide (LPS)-induced signaling pathways in mouse mammary epithelial cells (MEC). The pro-inflammatory cytokines were determined by ELISA. Nuclear factor-kappa B (NF-kappa B), inhibitory kappa B (I kappa B alpha) protein, p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and PPAR-gamma were determined by Western blotting. The results showed that emodin suppressed tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), iNOS and COX-2 expression. We also found that emodin inhibited LPS-induced NF-kappa B activation, IKB alpha degradation, phosphorylation of ERK, JNK and P38. Furthermore, emodin could activate PPAR-gamma and the anti-inflammatory effects of emodin can be reversed by GW9662, a specific antagonist for PPAR-gamma. In conclusion, our results demonstrate that emodin activates PPAR-gamma, thereby attenuating LPS-induced inflammatory response. (C) 2014 Elsevier B.V. All rights reserved.