肝纤维化是"肝炎－肝硬化－肝癌"三步曲中最关键的环节。而HSC激活是肝纤维化发生的中心环节，TGF-β1是启动邻近静息态HSC激活和转化的初始信号之一；PPARγ激动剂可激活PPARγ，抑制TGF-β-Smad信号及其下游CTGF和MMP-9等表达，有效地抑制肝纤维化的发生发展。在其过程中TGF-β-Smad- CTGF/PPARγ-c-Ski信号交联(cross talk)调节着肝纤维化的进程。荔枝核总黄酮(TFL)有调血脂、抗氧化和保肝作用，本课题组前期研究已证实TFL具有抗肝纤维化作用，因此，本课题从TGF-β-Smad/PPAR-γ信号通路交联角度出发，通过体内、外实验，运用Western Blot，RT-PCR等技术检测信号关键蛋白TβRⅠ、TβRⅡ、p300、CBP及下游CTGF、c-Ski、MMP2/9、TIMP-1、Ⅰ、Ⅲ型胶原表达，探讨TFL对上述信号交联的调节效应。

Hepatic fibrosis is critical in the three steps of hepatitis, hepatic cirrhosis and hepatic tumor. The activation of HSC is the key link in the process of hepatic fibrosis, while TGF-β1 is the first signal related to the activation and transformation of the neighboring resting HSC. PPARγ agonist can activate PPARγ and inhibit the signal of TGF-β-Smad and the expression of CTGF and MMP-9, stopping the development of hepatic fibrosis effectively. The signal crosstalk of TGF-β-Smad- CTGF/PPARγ-c-Ski controls the development of hepatic fibrosis. TFL is effective in regulating blood lipid, resisting oxidation and protecting liver, and it has been proven by our team that TFL is functional in resisting hepatic fibrosis. Based on the signal passway crosstalk between TGF-β-Smad and PPAR-γ and the in vitro and in vivo experiments, the techniques of Western Blot and RT-PCR are adopted here to detect the expressions of TβRⅠ, TβRⅡ, p300, CBP, CTGF, c-Ski, MMP2/9 and TIMP-1、Ⅰ、Ⅲ, with the purpose of discussing the regulating effect of TFL on the mentioned signal crosstalk.