Carnosic acid inhibits TLR4-MyD88 signaling pathway in LPS-stimulated 3T3-L1 adipocytes.
- Author:
Mi Young PARK
1
;
Seong Taek MUN
Author Information
- Publication Type:Original Article
- Keywords: 3T3-L1 adipocytes; carnosic acid; inflammation; toll-like receptor 4
- MeSH: Adipocytes*; Adipokines; Chemokine CCL2; Inflammation; Interleukin-6; Myeloid Differentiation Factor 88; Obesity; Phosphotransferases; RNA, Messenger; TNF Receptor-Associated Factor 6; Toll-Like Receptor 4; Tumor Necrosis Factor-alpha; Up-Regulation
- From:Nutrition Research and Practice 2014;8(5):516-520
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVES: Carnosic acid (CA), found in rosemary (Rosemarinus officinalis) leaves, is known to exhibit anti-obesity and anti-inflammatory activities. However, whether its anti-inflammatory potency can contribute to the amelioration of obesity has not been elucidated. The aim of the current study was to investigate the effect of CA on Toll-like receptor 4 (TLR4) pathways in the presence of lipopolysaccharide (LPS) in 3T3-L1 adipocytes. MATERIALS/METHODS: 3T3-L1 adipocytes were treated with CA (0-20 microM) for 1 h, followed by treatment with LPS for 30 min; mRNA expression of adipokines and protein expression of TLR4-related molecules were then measured. RESULTS: LPS-stimulated 3T3-L1 adipocytes showed elevated mRNA expression of tumor necrosis factor (TNF)-alpha, interleukin-6, and monocyte chemoattractant protein-1, and CA significantly inhibited the expression of these adipokine genes. LPS-induced up regulation of TLR4, myeloid differentiation factor 88, TNF receptor-associated factor 6, and nuclear factor-kappaB, as well as phosphorylated extracellular receptor-activated kinase were also suppressed by pre-treatment of 3T3-L1 adipocytes with CA. CONCLUSIONS: Results of this study suggest that CA directly inhibits TLR4-MyD88-dependent signaling pathways and decreases the inflammatory response in adipocytes.
