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丹酚酸B通过激活Nrf2信号通路抑制高脂饮食诱导的炎症反应。

Salvianolic Acid B Inhibits High-Fat Diet-Induced Inflammation by Activating the Nrf2 Pathway.

作者信息

Wang Bin, Sun Jin, Shi Yonghui, Le Guowei

机构信息

State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan Univ., Wuxi, Jiangsu, 214122, China.

出版信息

J Food Sci. 2017 Aug;82(8):1953-1960. doi: 10.1111/1750-3841.13808. Epub 2017 Jul 28.

DOI:10.1111/1750-3841.13808
PMID:28753232
Abstract

Salvianolic acid B (Sal B) is a major water-soluble bioactive component of Salvia miltiorrhiza, which is a traditional Chinese medicine. We investigated the ways in which Sal B affects high-fat diet (HFD)-induced immunological function disorder remission using a C57BL/6 mouse model. We gave groups of C57BL/6 mice a normal diet (Control), a normal diet supplemented with Sal B (Control + Sal B), a high-fat diet (HF), and a high-fat diet supplemented with Sal B (HF + Sal B) for 10 wk. Sal B supplementation decreased the body weight and plasma lipids, increased the fecal excretion of lipids, prevented the accumulation of chronic oxidative stress, and reversed the disproportionality of CD3 CD4 and CD3 CD8 T lymphocytes compared to HFD. We found an increase in IL-6 and TNF-α, while IL-10 decreased in plasma after the HFD and Sal B reversed the deregulation of the Thl/Th2 ratio. In addition, HFD-induced inflammation was stopped by Sal B through the downregulation of nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2), and inducible NO synthesis (iNOS), and the upregulation of nuclear factor-erythroid 2-related factor 2 (Nrf2)-regulated genes. These findings demonstrated that Sal B could effectively attenuate inflammation by activating the Nrf2-mediated antioxidant defense system.

摘要

丹酚酸B(Sal B)是传统中药丹参的主要水溶性生物活性成分。我们使用C57BL/6小鼠模型研究了Sal B影响高脂饮食(HFD)诱导的免疫功能障碍缓解的方式。我们将C57BL/6小鼠分为四组,分别给予正常饮食(对照组)、添加Sal B的正常饮食(对照组+Sal B)、高脂饮食(HF)和添加Sal B的高脂饮食(HF+Sal B),持续10周。与高脂饮食组相比,补充Sal B可降低体重和血脂,增加粪便脂质排泄,防止慢性氧化应激积累,并逆转CD3 CD4和CD3 CD8 T淋巴细胞的失衡。我们发现高脂饮食后血浆中IL-6和TNF-α增加,而IL-10减少,Sal B可逆转Th1/Th2比例的失调。此外,Sal B通过下调核因子-κB(NF-κB)、环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS),上调核因子红细胞2相关因子2(Nrf2)调控的基因,从而阻止高脂饮食诱导的炎症。这些发现表明,Sal B可通过激活Nrf2介导的抗氧化防御系统有效减轻炎症。

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