Aloe-emodin inhibits Pam3CSK4-induced MAPK and NF-kB signaling through TLR2 in macrophages
2016
Lee, M.J., Soonchunhyang University, Asan, Republic of Korea | Park, M.Y., Soonchunhyang University, Asan, Republic of Korea | Kim, S.K., Soonchunhyang University, Asan, Republic of Korea
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 Pam₃CSK₄for 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-alpha(TNF-alpha), interleukin-6 (IL-6), and interleukin-1beta (IL-1beta) in RAW 264.7 macrophages. Two concentrations of AE (10 micrometer and 20 micrometer) effectively reduced mRNA expression of TLR2 by 41.18% and 54.43%, respectively, compared to that in control cells (p less than 0.05). AE also decreased nuclear factor-kappa B (NF-kB) activation and mitogen-activated protein kinase (MAPK) phosphorylation. Phosphorylation levels of ERK1/2, p38, and JNK were markedly reduced by 20 micrometer 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-kB and MAPK signaling pathways in macrophages.
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