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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Published inCommunications biology Vol. 5; no. 1; pp. 519 - 15
Main Authors Zhou, Yingyu, Takano, Tomohiro, Li, Xuyang, Wang, Yimei, Wang, Rong, Zhu, Zhangliang, Tanokura, Masaru, Miyakawa, Takuya, Hachimura, Satoshi
Format Journal Article
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Published London Nature Publishing Group UK 31.05.2022
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Abstract 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.
AbstractList 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.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.
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.
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.
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.
ArticleNumber 519
Author Tanokura, Masaru
Li, Xuyang
Wang, Yimei
Wang, Rong
Miyakawa, Takuya
Takano, Tomohiro
Zhou, Yingyu
Hachimura, Satoshi
Zhu, Zhangliang
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  organization: Research Center for Food Safety, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo
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Snippet Macrophages are classified into classically activated M1 macrophages and alternatively activated M2 macrophages, and the two phenotypes of macrophages are...
β-elemene regulates the balance of proinflammatory cytokines in mouse white adipose tissue through MAPK signaling. Targets of β -elemene are predicted based on...
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SubjectTerms 13/21
13/31
13/95
38
38/39
631/154/1435/2163
692/699/1702/393
Adipose tissue
Animals
Ascites
Biology
Biomedical and Life Sciences
Body fat
Chronic illnesses
Cytokines
Cytokines - metabolism
Extracellular signal-regulated kinase
Gene expression
High fat diet
Inflammation
Inflammation - drug therapy
Inflammation - metabolism
Kinases
Life Sciences
Lipopolysaccharides
Macrophages
Macrophages - metabolism
MAP kinase
MAP Kinase Signaling System
Mice
Obesity
Obesity - drug therapy
Obesity - etiology
Obesity - metabolism
p38 Mitogen-Activated Protein Kinases - metabolism
Phenotypes
Phosphorylation
Protein kinase
Sesquiterpenes
Signal transduction
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Title β-elemene regulates M1-M2 macrophage balance through the ERK/JNK/P38 MAPK signaling pathway
URI https://link.springer.com/article/10.1038/s42003-022-03369-x
https://www.ncbi.nlm.nih.gov/pubmed/35641589
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https://www.proquest.com/docview/2672320378
https://pubmed.ncbi.nlm.nih.gov/PMC9156783
https://doaj.org/article/bb8c2be6cd51462298e8f1cf4938b29e
Volume 5
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