PMID- 23499696 OWN - NLM STAT- MEDLINE DCOM- 20131105 LR - 20220408 IS - 1879-0712 (Electronic) IS - 0014-2999 (Linking) VI - 705 IP - 1-3 DP - 2013 Apr 5 TI - Emodin ameliorates lipopolysaccharide-induced mastitis in mice by inhibiting activation of NF-kappaB and MAPKs signal pathways. PG - 79-85 LID - S0014-2999(13)00117-9 [pii] LID - 10.1016/j.ejphar.2013.02.021 [doi] AB - Emodin is an anthraquinone derivative from the Chinese herb Radix et Rhizoma Rhei. It has been reported that emodin possesses a number of biological properties, such as anti-inflammatory, anti-virus, anti-bacteria, anti-tumor, and immunosuppressive properties. However, the effect of emodin on mastitis is not yet known. The aim of this study was to investigate whether emodin has protective effect against lipopolysaccharide (LPS)-induced mastitis in a mouse model. The mouse model of mastitis was induced by injection of LPS through the duct of mammary gland. Emodin was administered intraperitoneally with the dose of 1, 2, and 4 mg/kg respectively 1h before and 12h after induction of LPS. Emodin significantly reduced infiltration of neutrophilic granulocyte, activation of myeloperoxidase (MPO), concentration of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1beta), and interleukin-6 (IL-6), mRNA expression levels of TNF-alpha, IL-1beta and IL-6, which were increased in LPS-induced mouse mastitis. In addition, emodin influenced nuclear factor kappa-B signal transduction pathway by inhibiting activation of nuclear transcription factor-kappaB (NF-kappaB) p65 and degradation inhibitor of NF-kappaB alpha (IkappaBalpha), and emodin also influenced mitogen activated protein kinases signal transduction pathway by depression activation of p38, extracellular signal-regulated kinase (ERK), and c-jun NH2-terminal kinase (JNK). In conclusion, these results indicated that emodin could exert beneficial effects on experimental mastitis induced by LPS and may represent a novel treatment strategy for mastitis. CI - Copyright (c) 2013 Elsevier B.V. All rights reserved. FAU - Li, Depeng AU - Li D AD - Department of Clinical Veterinary Medicine, College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin Province 130062, People's Republic of China. FAU - Zhang, Naisheng AU - Zhang N FAU - Cao, Yongguo AU - Cao Y FAU - Zhang, Wen AU - Zhang W FAU - Su, Gaoli AU - Su G FAU - Sun, Yong AU - Sun Y FAU - Liu, Zhicheng AU - Liu Z FAU - Li, Fengyang AU - Li F FAU - Liang, Dejie AU - Liang D FAU - Liu, Bo AU - Liu B FAU - Guo, Mengyao AU - Guo M FAU - Fu, Yunhe AU - Fu Y FAU - Zhang, Xichen AU - Zhang X FAU - Yang, Zhengtao AU - Yang Z LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20130313 PL - Netherlands TA - Eur J Pharmacol JT - European journal of pharmacology JID - 1254354 RN - 0 (Anti-Inflammatory Agents) RN - 0 (Cytokines) RN - 0 (Lipopolysaccharides) RN - 0 (NF-kappa B) RN - 0 (RNA, Messenger) RN - EC 1.11.1.7 (Peroxidase) RN - KA46RNI6HN (Emodin) SB - IM MH - Animals MH - Anti-Inflammatory Agents/*pharmacology/therapeutic use MH - Cytokines/genetics/metabolism MH - Emodin/*pharmacology/therapeutic use MH - Female MH - Gene Expression Regulation/drug effects MH - Lipopolysaccharides MH - MAP Kinase Signaling System/*drug effects MH - Male MH - Mastitis/chemically induced/drug therapy/*metabolism/pathology MH - Mice MH - Mice, Inbred BALB C MH - NF-kappa B/*antagonists & inhibitors MH - Peroxidase/metabolism MH - RNA, Messenger/metabolism EDAT- 2013/03/19 06:00 MHDA- 2013/11/06 06:00 CRDT- 2013/03/19 06:00 PHST- 2012/10/05 00:00 [received] PHST- 2013/02/04 00:00 [revised] PHST- 2013/02/07 00:00 [accepted] PHST- 2013/03/19 06:00 [entrez] PHST- 2013/03/19 06:00 [pubmed] PHST- 2013/11/06 06:00 [medline] AID - S0014-2999(13)00117-9 [pii] AID - 10.1016/j.ejphar.2013.02.021 [doi] PST - ppublish SO - Eur J Pharmacol. 2013 Apr 5;705(1-3):79-85. doi: 10.1016/j.ejphar.2013.02.021. Epub 2013 Mar 13.