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乌龙茶茶黄素的抗炎活性及分子机制

Anti-inflammatory activity and molecular mechanism of Oolong tea theasinensin.

作者信息

Hisanaga Ayami, Ishida Hisako, Sakao Kozue, Sogo Takayuki, Kumamoto Takuma, Hashimoto Fumio, Hou De-Xing

机构信息

United Graduate School of Agricultural Science, Faculty of Agriculture, Kagoshima University, Korimoto 1-21-24, Kagoshima, 890-0065, Japan.

出版信息

Food Funct. 2014 Aug;5(8):1891-7. doi: 10.1039/c4fo00152d.

Abstract

Oolong tea theasinensins are a group of tea polyphenols different from green tea catechins and black tea theaflavins, and they are considered as bioactive compounds in Oolong tea. In the present study, based on the properties of theasinensin and information about inflammatory processes, we investigated the anti-inflammatory activity and molecular mechanisms of theasinensin A (TSA) in both cell and animal models. In the cell model, TSA reduced the levels of pro-inflammatory mediators including inducible nitric oxide synthase (iNOS), nitric oxide (NO), interleukin-12 (IL-12) (p70), tumor necrosis factor alpha (TNF-α), and monocyte chemotactic protein-1 (MCP-1) induced by lipopolysaccharide (LPS). Cellular signaling analysis revealed that TSA downregulated MAPK/ERK kinase (MEK)-extracellular signal-regulated kinase (ERK) signaling. Pull-down assay and affinity data revealed that TSA might directly bind to MEK-ERK for the inhibitory action. In the animal model, TSA suppressed the production of IL-12 (p70), TNF-α, and MCP-1 and attenuated mouse paw edema induced by LPS.

摘要

乌龙茶茶黄素是一类不同于绿茶儿茶素和红茶茶黄素的茶多酚,它们被认为是乌龙茶中的生物活性化合物。在本研究中,基于茶黄素的特性以及炎症过程的相关信息,我们在细胞和动物模型中研究了茶黄素A(TSA)的抗炎活性及其分子机制。在细胞模型中,TSA降低了由脂多糖(LPS)诱导的促炎介质水平,包括诱导型一氧化氮合酶(iNOS)、一氧化氮(NO)、白细胞介素-12(IL-12)(p70)、肿瘤坏死因子-α(TNF-α)和单核细胞趋化蛋白-1(MCP-1)。细胞信号分析表明,TSA下调了丝裂原活化蛋白激酶/细胞外信号调节激酶(MEK)-细胞外信号调节激酶(ERK)信号通路。下拉试验和亲和力数据表明,TSA可能直接与MEK-ERK结合以发挥抑制作用。在动物模型中,TSA抑制了IL-12(p70)、TNF-α和MCP-1的产生,并减轻了LPS诱导的小鼠爪肿胀。

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