Center for Gene and Cell Engineering, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China,
Eur J Nutr. 2014 Feb;53(1):187-99. doi: 10.1007/s00394-013-0516-8. Epub 2013 Mar 21.
To investigate the protective mechanisms of an 85 % pure extract of (-) epigallocatechin gallate (EGCG) in the development of fibrosis, oxidative stress and inflammation in a recently developed dietary-induced animal model of non-alcoholic fatty liver disease (NAFLD).
Female Sprague-Dawley rats were fed with either normal rat diet or high-fat diet for 8 weeks to develop NAFLD. For both treatments, rats were treated with or without EGCG (50 mg/kg, i.p. injection, 3 times per week). At the end, blood and liver tissue samples were obtained for histology, molecular, and biochemical analyses.
Non-alcoholic fatty liver disease (NAFLD) rats showed significant amount of fatty infiltration, necrosis, fibrosis, and inflammation. This was accompanied by a significant expressional increase in markers for fibrosis, oxidative stress, and inflammation. TGF/SMAD, PI3 K/Akt/FoxO1, and NF-κB pathways were also activated. Treatment with EGCG improved hepatic histology (decreased number of fatty score, necrosis, and inflammatory foci), reduced liver injury (from ~0.5 to ~0.3 of ALT/AST ratio), attenuated hepatic changes including fibrosis (reduction in Sirius Red and synaptophysin-positive stain) with down-regulation in the expressions of key pathological oxidative (e.g. nitrotyrosine formation) and pro-inflammatory markers (e.g. iNOS, COX-2, and TNF-α). EGCG treatment also counteracted the activity of TGF/SMAD, PI3 K/Akt/FoxO1, and NF-κB pathways. Treatment with EGCG did not affect the healthy rats.
Epigallocatechin gallate (EGCG) reduced the severity of liver injury in an experimental model of NAFLD associated with lower concentration of pro-fibrogenic, oxidative stress, and pro-inflammatory mediators partly through modulating the activities of TGF/SMAD, PI3 K/Akt/FoxO1, and NF-κB pathways. Therefore, green tea polyphenols and EGCG are useful supplements in the prevention of NAFLD.
研究 85%纯度（-）表没食子儿茶素没食子酸酯（EGCG）提取物在新近开发的非酒精性脂肪性肝病（NAFLD）动物模型中对纤维化、氧化应激和炎症发展的保护机制。
雌性 Sprague-Dawley 大鼠分别用正常大鼠饲料或高脂肪饲料喂养 8 周以建立 NAFLD。对于两种治疗方法，大鼠分别用或不用 EGCG（50mg/kg，腹腔注射，每周 3 次）治疗。最后，采集血液和肝组织样本进行组织学、分子和生化分析。
非酒精性脂肪性肝病（NAFLD）大鼠表现出明显的脂肪浸润、坏死、纤维化和炎症。这伴随着纤维化、氧化应激和炎症标志物的显著表达增加。TGF/SMAD、PI3 K/Akt/FoxO1 和 NF-κB 途径也被激活。EGCG 治疗改善了肝组织学（减少脂肪评分、坏死和炎症灶的数量），降低了肝损伤（ALT/AST 比值从0.5 降至0.3），减轻了肝纤维化（减少天狼星红和突触素阳性染色）以及关键病理氧化（如硝基酪氨酸形成）和促炎标志物（如 iNOS、COX-2 和 TNF-α）的表达下调。EGCG 治疗还抑制了 TGF/SMAD、PI3 K/Akt/FoxO1 和 NF-κB 途径的活性。EGCG 治疗对健康大鼠没有影响。
表没食子儿茶素没食子酸酯（EGCG）通过调节 TGF/SMAD、PI3 K/Akt/FoxO1 和 NF-κB 途径的活性，降低了 NAFLD 实验模型中肝损伤的严重程度，与较低浓度的促纤维化、氧化应激和促炎介质有关。因此，绿茶多酚和 EGCG 可作为预防 NAFLD 的有用补充剂。
