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迷迭香酸抑制 LPS 刺激的 3T3-L1 脂肪细胞中 TLR4-MyD88 信号通路。

Carnosic acid inhibits TLR4-MyD88 signaling pathway in LPS-stimulated 3T3-L1 adipocytes.

机构信息

Department of Food & Nutrition Education, Graduate School of Education, Soonchunhyang University, Asan, Chungnam 336-745, Korea.

Department of Obstetrics and Gynecology, Soonchunhyang University Cheonan Hospital, Soonchunhyang-6-gil 31, Dongnam-gu, Cheonan 330-721, Korea.

出版信息

Nutr Res Pract. 2014 Oct;8(5):516-20. doi: 10.4162/nrp.2014.8.5.516. Epub 2014 Jun 30.

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 µM) 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)-α, 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-κB, 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.

摘要

背景/目的:迷迭香(Rosemarinus officinalis)叶中的迷迭香酸(CA)具有抗肥胖和抗炎活性。然而,其抗炎效力是否有助于改善肥胖尚未阐明。本研究旨在探讨 CA 在 3T3-L1 脂肪细胞中存在脂多糖(LPS)时对 Toll 样受体 4(TLR4)途径的影响。

材料/方法:用 CA(0-20 μM)处理 3T3-L1 脂肪细胞 1 小时,然后用 LPS 处理 30 分钟;然后测量脂肪因子的 mRNA 表达和 TLR4 相关分子的蛋白表达。

结果

LPS 刺激的 3T3-L1 脂肪细胞表现出肿瘤坏死因子(TNF)-α、白细胞介素-6 和单核细胞趋化蛋白-1 的 mRNA 表达升高,CA 显著抑制这些脂肪因子基因的表达。CA 预处理还抑制了 LPS 诱导的 TLR4、髓样分化因子 88、TNF 受体相关因子 6 和核因子-κB 的上调,以及细胞外受体激活激酶的磷酸化。

结论

本研究结果表明,CA 直接抑制 TLR4-MyD88 依赖性信号通路,并降低脂肪细胞的炎症反应。

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