中文摘要：

内毒素 lipopolysaccharide (LPS ) 作为第二攻击在肝炎的煽动性的反应的加速起一个重要作用。能由指向 LPS 阻止发炎的混合物有潜在的治疗学的临床的申请。Epigallocatechin-3-gallate (EGCG ) 有有势力 hepatocyte 保护的效果和温和反肝炎病毒工作。这里，我们调查了 EGCG 是否在刺激 LPS 的 L02 hepatocytes 稀释了煽动性的反应的严厉。L02 hepatocytes 是有为 2 h 的 EGCG 的 pretreated，然后在 250 ng/ml 由 LPS 刺激了。 chemokine 的表示层次在表示并且藏匿的激活正常T房间( Rantes )和单核白血球之上调整了趋化性的 protein-1 ( MCP-1 )， 支持inflammatory cytokines 肿瘤坏死因素--(TNF-)并且干扰素--，粘附分子细胞间的粘附 molecule-1 ( ICAM-1 )，氧化剂压力分子氮的氧化物(没有)，脉管的 endothelial 生长因素( VEGF )，和矩阵 metalloproteinase-2 ( MMP-2 )被连接酶的 immunosorbent 试金测试。全部的细胞外的调整信号的 kinase 1/2 (ERK1/2 ) 的表示， phospho-ERK1/2 (p-ERK1/2 ) ， p-AKT，全部的 p38， phospho-p38 (p-p38 ) ，全部的 p65 和 phospho-p65 (p-p65 ) ， IB， phospho-IB (p-IB ) 和 TNF 受体联系了因素 2 被西方的污点分析测试。我们的结果证明有 EGCG 的那个预告的处理能显著地减少 TNF- 的生产， Rantes， MCP-1， ICAM-1，不在以一种剂量依赖者方式的刺激 LPS 的 L02 hepatocytes 的 VEGF，和 MMP-2。EGCG 的效果可能与原子 factor-B (NF-B ) 和由 p-IB， p65， p-p65， p-p38， p-ERK1/2，和 p-AKT 的下面规定表明小径的激活 mitogen 的蛋白质 kinase (MAPK ) 的抑制有关。这些结果显示 EGCG 压制导致 LPS 的煽动性的反应和氧化剂应力并且由禁止 NF-B 和 MAPK 小径部分施加它的 hepatocyte 保护的活动。

英文摘要：

Endotoxin lipopolysaccharide （LPS） plays an important role in the acceleration of inflammatory reaction of hepa- titis as the second attack. Compounds that can prevent in- flammation by targeting LPS have potential therapeutic clinical application. Epigallocatechin-3-gallate （EGCG） has potent hepatocyte-protective effect and mild anti-hepatitis virus function. Here, we investigated whether EGCG attenuated the severity of inflammatory response in LPS-stimulated L02 hepatocytes. L02 hepatocytes were pretreated with EGCG for 2 h, then stimulated by LPS at 250 ng/ml. The expression levels of chemokine regulated upon activation normal T-cell expressed and secreted （Rantes） and monocyte chemotactic protein-1 （MCP-1）, pro-inflammatory cytokines tumor necrosis factor-α （TNF-α and interferon-% adhesion molecule intercellular adhesion molecule-1 （ICAM-1）, oxidant stress molecules nitric oxide （NO）, vascular endothelial growth factor （VEGF）, and matrix metaHoproteinase-2 （MMP-2） were tested by enzyme-linked immunosorbent assay. The expression of total extracellular signal-regulated kinase 1/2 （ERK1/2）, phospho-ERK1/2 （p-ERK1/2）, p-AKT, total p38, phospho-p38 （p-p38）, total p65 and phospho-p65 （p-p65）, IκBα, phospho-IκBα（p-IκBα and TNF receptor associated factor 2 were tested by western blot analysis. Our results showed that pre-treatment with EGCG could significantly reduce the production of TNF-α, Rantes, MCP-1, ICAM-1, NO, VEGF, and MMP-2 in LPS-stimulated L02 hepatocytes in a dose-dependent manner. The effect of EGCG may be related to the inhibition of nuclear factor-κB （NF-κB） and mitogen-activated protein kinase （MAPK） signaling pathways by down-regulation of p-IκBα, p65, p-p65, p-p38, p-ERK1/2, and p-AKT. These results indicate that EGCG suppresses LPS-induced inflammatory response and oxidant stress and exerts its hepatocyte-protective activity partially by inhibiting NF-κB and MAPK pathways.