四氯化碳
肝星状细胞
肝纤维化
羟脯氨酸
化学
纤维化
四氯化碳
没食子酸表没食子酸酯
肝损伤
药理学
基质金属蛋白酶
谷胱甘肽
生物化学
抗氧化剂
内科学
内分泌学
多酚
医学
酶
有机化学
作者
Zhen Mao,Qing Wang,Xiaobin Huang,Luxi Cao,Xi Chen,Kening Sun,Yi Liu,Wenqian Li,Lu Zhang
标识
DOI:10.1016/j.jnutbio.2006.12.016
摘要
The aim of the study was to examine the effects of epigallocatechin-3-gallate (EGCG) on hepatic fibrogenesis and on cultured hepatic stellate cells (HSCs). The rat model of carbon tetrachloride (CCl4)-induced hepatic fibrosis was used to assess the effect of daily intraperitoneal injections of EGCG on the indexes of fibrosis. Histological and hepatic hydroxyproline examination revealed that EGCG significantly arrested progression of hepatic fibrosis. EGCG caused significant amelioration of liver injury (reduced activities of serum alanine aminotransferase and aspartate aminotransferase). The development of CCl4-induced hepatic fibrosis altered the redox state with a decreased hepatic glutathione and increased the formation of lipid peroxidative products, which were partially normalized by treatment with EGCG, respectively. Moreover, EGCG markedly attenuated HSC activation as well as matrix metalloproteinase (MMP)-2 activity. In cultured stellate cell, the expression of MMP-2 mRNA and protein were substantially reduced by EGCG treatment. Concanavalin A-induced activation of secreted MMP-2 was inhibited by EGCG through the influence of membrane type 1-MMP activity. These results demonstrate that administration of EGCG may be useful in the treatment and prevention of hepatic fibrosis.
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