Aloe-emodin inhibits Pam₃CSK₄-induced MAPK and NF-κB signaling through TLR2 in macrophages.
10.4163/jnh.2016.49.4.241
- Author:
Mi Jin LEE
1
;
Mi Young PARK
;
Soon Kyung KIM
Author Information
1. Department of Food Science and Nutrition, College of Natural Science, Soonchunhyang University, Asan 31538, Korea. soon56@sch.ac.kr
- Publication Type:Original Article
- Keywords:
Aloe-emodin (AE);
macrophage;
mitogen-activated protein kinase (MAPK);
nuclear factorkappa B (NF-κB);
Toll-like receptor 2 (TLR2)
- MeSH:
Aloe;
Cytokines;
In Vitro Techniques;
Interleukin-6;
Macrophages*;
Necrosis;
Phosphorylation;
Protein Kinases;
RNA, Messenger
- From:Journal of Nutrition and Health
2016;49(4):241-246
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
