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KMID : 1036720160490040241
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Journal of Nutrition and Health
2016 Volume.49 No. 4 p.241 ~ p.246
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Aloe-emodin inhibits Pam3CSK4-induced MAPK and NF-κB signaling through TLR2 in macrophages
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Lee Mi-Jin
Park Mi-Young
Kim Soon-Kyung
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Abstract
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Purpose: Aloe-emodin (AE), an ingredient of aloe, is known to exhibit anti-inflammatory activities. However, little is known
about the underlying molecular mechanisms of its inflammatory modulatory activity in vitro. In the present study, we
investigated the anti-inflammatory potential of AE using Pam3CSK4-stimulated macrophages.
Methods: RAW 264.7 macrophages were treated with AE (0~20 mM) for 1 h, followed by treatment with Pam3CSK4 for 1 h. After incubation, mRNA expression levels of cytokines were measured. The effect of AE on TLR2-related molecules was also investigated in Pam3CSK4-stimulated RAW 264.7 macrophages.
Results: AE attenuated Pam3CSK4-stimulated expression of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in RAW 264.7 macrophages. Two concentrations of AE (10 μM and 20 μM) effectively reduced mRNA expression of TLR2 by 41.18% and 54.43%, respectively, compared to that in control cells (p < 0.05). AE also decreased nuclear factor-kappa B (NF-κB) activation and mitogen-activated protein kinase (MAPK) phosphorylation. Phosphorylation levels of ERK1/2, p38, and JNK were markedly reduced by 20 μM AE. In particular, AE decreased phosphorylation of ERK in a dose-dependent manner in Pam3CSK4-stimulated RAW 264.7 macrophages.
Conclusion: Our data indicate that AE exerts its anti-inflammatory effect by suppressing TLR2-mediated activation of NF-κB and MAPK signaling pathways in macrophages.
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KEYWORD
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Aloe-emodin (AE), macrophage, mitogen-activated protein kinase (MAPK), nuclear factorkappa B (NF-κB), Toll-like receptor 2 (TLR2)
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