Neutrophil, restraint by green tea:: Inhibition of inflammation, associated angiogenesis, and pulmonary fibrosis

Neutrophil, restraint by green tea:: Inhibition of inflammation, associated angiogenesis, and pulmonary fibrosis
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DOI:
10.4049/jimmunol.170.8.4335
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发表时间:
2003-04-15
影响因子:
4.4
通讯作者:
Garbisa, S
Garbisa, S
中科院分区:
医学2区
文献类型:
--
作者:
Donà, M;Dell'Aica, I;Garbisa, S

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中性粒细胞在宿主防御和炎症中发挥重要作用,但后者可能引发和维持一系列急性和慢性疾病的发病机制。绿色茶已被声称通过未知的分子机制发挥抗炎特性。我们先前已经表明,绿色茶中最丰富的儿茶素,(-)表没食子儿茶素-3-没食子酸酯(EGCG),强烈抑制中性粒细胞弹性蛋白酶。在这里,我们发现1)微摩尔EGCG抑制活性氧活性和抑制活化的中性粒细胞的凋亡,2)显着抑制趋化因子诱导的中性粒细胞的体外趋化性; 3)口服EGCG和绿色茶提取物都在体内阻断炎性血管生成模型中嗜铬粒细胞介导的血管生成,和4)口服施用绿色茶提取物增强肺部炎症模型中的消退,显著地减少了随后的纤维化。这些结果提供了对绿色茶所声称的有益特性的分子和细胞见解,并表明EGCG是具有治疗潜力的有效抗炎化合物。
Neutrophils play an essential role in host defense and inflammation, but the latter may trigger and sustain the pathogenesis of a range of acute and chronic diseases. Green tea has been claimed to exert anti-inflammatory properties through unknown molecular mechanisms. We have previously shown that the most abundant catechin of green tea, (-)epigallocatechin-3-gallate (EGCG), strongly inhibits neutrophil elastase. Here we show that 1) micromolar EGCG represses reactive oxygen species activity and inhibits apoptosis of activated neutrophils, and 2) dramatically inhibits chemokine-induced neutrophil chemotaxis in vitro; 3) both oral EGCG and green tea extract block neutrophil-mediated angiogenesis in vivo in an inflammatory angiogenesis model, and 4) oral administration of green tea extract enhances resolution in a pulmonary inflammation model, significantly reducing consequent fibrosis. These results provide molecular and cellular insights into the claimed beneficial properties of green tea and indicate that EGCG is a potent anti-inflammatory compound with therapeutic potential.