Department of Nutritional Sciences, University of Connecticut, Storrs, CT, USA.
J Nutr. 2012 Jan;142(1):57-63. doi: 10.3945/jn.111.148544. Epub 2011 Dec 7.
Nonalcoholic steatohepatitis (NASH) is characterized by oxidative stress and inflammatory responses that exacerbate liver injury. The objective of this study was to determine whether the antioxidant and antiinflammatory activities of green tea extract (GTE) would protect against NASH in a model of diet-induced obesity. Adult Wistar rats were fed a low-fat (LF) diet or high-fat (HF) diet containing no GTE or GTE at 1% or 2% (HF+2GTE) for 8 wk. The HF group had greater (P ≤ 0.05) serum alanine (ALT) and aspartate aminotransferases and hepatic lipids than the LF group. Both GTE groups had lower ALT and hepatic lipid than the HF group. In liver and epididymal adipose, the HF group had lower glutathione as well as greater mRNA and protein expression of TNFα and monocyte chemoattractant protein-1 (MCP-1) and NFκB binding activity than the LF group. Compared to the HF group, the HF+2GTE group had greater glutathione and lower protein and mRNA levels of inflammatory cytokines in both tissues. NFκB binding activities at liver and adipose were also lower, likely by inhibiting the phosphorylation of inhibitor of NFκB. NFκB binding activities in liver and adipose (P ≤ 0.05; r = 0.62 and 0.46, respectively) were correlated with ALT, and hepatic NFκB binding activity was inversely related to liver glutathione (r = -0.35). These results suggest that GTE-mediated improvements in glutathione status are associated with the inhibition of hepatic and adipose inflammatory responses mediated by NFκB, thereby protecting against NASH.
非酒精性脂肪性肝炎（NASH）的特征是氧化应激和炎症反应，这些反应会加剧肝损伤。本研究的目的是确定绿茶提取物（GTE）的抗氧化和抗炎活性是否能预防饮食诱导肥胖模型中的 NASH。成年 Wistar 大鼠分别用低脂（LF）饮食或高脂肪（HF）饮食（不含 GTE 或含 1%或 2%GTE）喂养 8 周。HF 组的血清丙氨酸（ALT）和天冬氨酸转氨酶以及肝脂质均高于 LF 组（P≤0.05）。与 HF 组相比，GTE 组的 ALT 和肝脂质均较低。在肝脏和附睾脂肪组织中，HF 组的谷胱甘肽水平较低，TNFα 和单核细胞趋化蛋白-1（MCP-1）的 mRNA 和蛋白表达以及 NFκB 结合活性均高于 LF 组。与 HF 组相比，HF+2GTE 组在这两种组织中的谷胱甘肽水平较高，炎症细胞因子的蛋白和 mRNA 水平较低。NFκB 在肝脏和脂肪组织中的结合活性也较低，这可能是通过抑制 NFκB 的磷酸化来实现的。NFκB 在肝脏和脂肪组织中的结合活性（P≤0.05；r=0.62 和 0.46）与 ALT 呈正相关，而肝脏 NFκB 结合活性与肝脏谷胱甘肽呈负相关（r=-0.35）。这些结果表明，GTE 介导的谷胱甘肽状态的改善与 NFκB 介导的肝和脂肪炎症反应的抑制有关，从而防止了 NASH 的发生。
