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Aloe‐emodin attenuates inflammatory signaling cascade in Pam 3 CSK 4 ‐stimulated macrophages
Author(s) -
Park MiYoung,
Kim SoonKyung
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.166.7
Subject(s) - aloe emodin , tlr2 , proinflammatory cytokine , mapk/erk pathway , chemistry , tumor necrosis factor alpha , p38 mitogen activated protein kinases , signal transduction , nf κb , kinase , macrophage , pharmacology , microbiology and biotechnology , inflammation , emodin , in vitro , immunology , biochemistry , biology , tlr4
Aloe‐emodin (AE) is an ingredient of aloe and is known to exhibit anti‐inflammatory activities. However, little is known about underlying molecular mechanisms of inflammatory modulation in vitro. In the present study, we investigated the anti‐inflammatory potential of AE using Pam 3 CSK 4 ‐stimulated macrophages. RAW 264.7 macrophages was treated with AE (0–20 mM) for 1 h followed by Pam 3 CSK 4 for 1 h, and then the mRNA expression levels of cytokines were measured. The effect of AE on the TLR2‐related molecules was also investigated in Pam 3 CSK 4 ‐stimulated RAW264.7 macrophages. AE attenuated Pam 3 CSK 4 ‐stimulated expression of proinflammatory cytokines, including tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), and interleukin‐1β (IL‐1β) in both RAW264.7 macrophages and DMEMs. AE showed reduction on mRNA levels of toll‐like receptor 2 (TLR2) and on activation of the nuclear factor‐kappa B (NF‐κB) and mitogen‐activated protein kinase (MAPK) phosphorylation. Our data suggest that AE exerts its anti‐inflammatory effect by suppressing the TLR2‐mediated of NF‐κB and MAPK signaling pathways in macrophages. Support or Funding Information This study was supported by Soonchunhyang University Research Fund.