Baicalin inhibits macrophage activation by lipopolysaccharide and protects mice from endotoxin shock
Baicalin inhibits macrophage activation by lipopolysaccharide and protects mice from endotoxin shock
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DOI：
10.1016/j.bcp.2007.10.009
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发表时间：
2008-02-15
影响因子：
5.8
通讯作者：
Ren, Jin
中科院分区：
文献类型：
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作者：
Liu, Lin-Lin;Gong, Li-Kun;Ren, Jin
黄芩苷（Baicalin，BA）在体内外均具有抗炎作用，用于治疗炎症性疾病。在这里，我们报告BA抑制巨噬细胞的活化，并保护小鼠免受巨噬细胞介导的内毒素休克。体外实验表明，BA可抑制LPS或IFN-γ诱导的RAW264.7细胞和腹腔巨噬细胞NO生成和诱导型一氧化氮合酶（iNOS）表达的增加，但对iNOS活性无直接影响。同样，BA抑制活性氧化物质（ROS）的产生，而增加细胞内超氧化物歧化酶（SOD）的水平。此外，BA抑制由脂多糖（LPS）诱导的RAW264.7细胞中的炎症介质包括肿瘤坏死因子（TNF）-α、内皮素（ET）-1和TXA 2（TXA 2）的产生。在动物模型中，BA可能通过抑制细胞因子和NO的产生而对D-氨基半乳糖（D-GalN）/LPS诱导的内毒素休克小鼠产生保护作用。BA抑制巨噬细胞产生炎症介质，可能是治疗巨噬细胞介导疾病的潜在靶点。(c)2007年爱思唯尔公司All rights reserved.
Baicalin (BA) exhibits anti-inflammatory effect in vivo and in vitro and is used to treat inflammatory diseases. Here, we report that BA inhibits the activation of macrophage and protects mice from macrophage-mediated endotoxin shock. The experiments in vitro showed BA suppressed the increased generation of nitric oxide (NO) and expression of inducible nitric oxide synthase (iNOS) induced by LPS or Interferon-gamma (IFN-gamma) without directly affecting iNOS activity in RAW264.7 cells and peritoneal macrophages. Similarly, BA inhibited the production of reactive oxidative species (ROS), whereas augmented the level of intracellular superoxide dismutase (SOD). Moreover, BA inhibited the production of inflammatory mediators including tumor necrosis factor (TNF)-alpha, endothelin (ET)-1 and thromboxane A(2) (TXA(2)) induced by lipopolysaccharide (LPS) in RAW264.7 cells. In animal model, BA protected mice from endotoxin shock induced by D-galactosamine (D-GalN)/LPS possibly through inhibiting the production of cytokine and NO. Collectively, BA inhibited the production of inflammatory mediators by macrophage and may be a potential target for treatment of macrophage-mediated diseases. (c) 2007 Elsevier Inc. All rights reserved.