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

被引:89
作者
Yang, Zhengtao [1 ]
Zhou, Ershun [1 ]
Wei, Dong [1 ]
Li, Depeng [1 ]
Wei, Zhengkai [1 ]
Zhang, Wen [1 ]
Zhang, Xicheu [1 ]
机构
[1] Jilin Univ, Coll Vet Med, Changchun 130062, Jilin Province, Peoples R China
基金
中国国家自然科学基金;
关键词
Emodin; NF-kappa B; PPAR-gamma; Cytokines; LPS; Mastitis; NF-KAPPA-B; ACUTE LUNG INJURY; CYTOKINE EXPRESSION; TRANSCRIPTION FACTORS; RECEPTOR; INNATE; LIPOPOLYSACCHARIDE; INFECTIONS; IMMUNITY; KINASE;
D O I
10.1016/j.intimp.2014.05.019
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
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.
引用
收藏
页码:354 / 360
页数:7
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