β-elemene regulates M1-M2 macrophage balance through the ERK/JNK/P38 MAPK signaling pathway

Macrophages are classified into classically activated M1 macrophages and alternatively activated M2 macrophages, and the two phenotypes of macrophages are present during the development of various chronic diseases, including obesity-induced inflammation. In the present study, β-elemene, which is con...

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Veröffentlicht in:Communications biology 2022-05, Vol.5 (1), p.519-519, Article 519
Hauptverfasser: Zhou, Yingyu, Takano, Tomohiro, Li, Xuyang, Wang, Yimei, Wang, Rong, Zhu, Zhangliang, Tanokura, Masaru, Miyakawa, Takuya, Hachimura, Satoshi
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Sprache:eng
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Zusammenfassung:Macrophages are classified into classically activated M1 macrophages and alternatively activated M2 macrophages, and the two phenotypes of macrophages are present during the development of various chronic diseases, including obesity-induced inflammation. In the present study, β-elemene, which is contained in various plant substances, is predicted to treat high-fat diet (HFD)-induced macrophage dysfunction based on the Gene Expression Omnibus (GEO) database and experimental validation. β-elemene impacts the imbalance of M1-M2 macrophages by regulating pro-inflammatory cytokines in mouse white adipose tissue both in vitro and in vivo. In addition, the RAW 264 cell line, which are macrophages from mouse ascites, is used to identify the effects of β-elemene on inhibiting bacterial endotoxin lipopolysaccharide (LPS)-induced phosphorylation of mitogen-activated protein kinase (MAPK) pathways. These pathways both induce and are activated by pro-inflammatory cytokines, and they also participate in the process of obesity-induced inflammation. The results highlight that β-elemene may represent a possible macrophage-mediated therapeutic medicine. β-elemene regulates the balance of proinflammatory cytokines in mouse white adipose tissue through MAPK signaling. Targets of β -elemene are predicted based on its 3D structure and include regulators of macrophage-mediated processes.
ISSN:2399-3642
2399-3642
DOI:10.1038/s42003-022-03369-x