Baicalin inhibits macrophage activation by lipopolysaccharide and protects mice from endotoxin shock |
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Authors: | Liu Lin-lin Gong Li-kun Wang Hui Xiao Ying Wu Xiong-fei Zhang Yun-hai Xue Xiang Qi Xin-ming Ren Jin |
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Affiliation: | State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201203, China. |
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Abstract: | 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 A2 (TXA2) 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. |
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Keywords: | Baicalin Macrophage Lipopolysaccharide Nitric oxide Endotoxin shock |
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