肝硬化-肝癌癌前病变的恶性转变导致肝癌的形成。大量文献证明，TGF-β1调控肝癌前病变细胞、炎症纤维化微环境的产生以及相互促进，TGF-β1/Smad2/3通路具有促癌/抑癌两个相反作用，而发挥哪种作用依赖于Smad2/3的信号提取转换，Smad3双重信号转变（p-Smad3C/p21和p-Smad3L/c-Myc）是该通路发挥抑癌/促癌作用的关键，但该通路调控肝硬化-肝癌癌前病变恶变的机制不十分清楚。本课题拟采用动物和细胞实验，通过检测TGF-β1/Smad2/3通路因子、下游c-Myc、p21表达，探究TGF-β1/Smad2/3通路对肝硬化-肝癌癌前病变恶变的调控作用。益脾养肝方是防治肝硬化进展的验方，前期研究发现该方对肝癌前病变亦有抑制作用，本研究进一步探究该方是否通过调控TGF-β1/Smad2/3通路，发挥阻断或逆转肝硬化-肝癌癌前病变恶变的作用，为中医药防治肝癌开辟新思路。

The malignant transformation of hepatic cirrhosis-precancerous lesion progressively can result in hepatic carcinoma ultimately. Plenty of studies have found that TGF-β1 can regulate precancerous cells, inflammatory and fibrotic microenvironment, and the interaction between them. TGF-β1/Smad2/3 pathway has both tumor suppressive and oncogenic activities. Smad2/3 mainly transfer TGF-β1’s ecto-signal into cell nucleus. Smad3 double signal transduction pathways (p-Smad3C/p21 and p-Smad3L/c-Myc) play an important role for tumor suppressive and oncogenic activities. Therefore, TGF-β1/Smad2/3 pathway may regulate the malignant transformation of hepatic cirrhosis-precancerous lesion, but the mechanism is not very clear. This study intends to adopt the method of rats and cells experiment, to discuss on TGF-β1/Smad2/3 signaling pathway ’s in regulating malignant transformation of hepatic cirrhosis-precancerous lesion by detecting the cytokines expression of TGF-β1/Smad2/3 pathway, c-Myc and p21. YiPiYangGanFang is effective for treatment of liver cirrhosis progress. Our previous study found that YiPiYangGanFang can ameliorate the pathologic change of hepatic precancerous lesion in rats induced by DEN. This study is to explore further whether the YiPiYangGanFang could block or reverse the malignant transformation of hepatic cirrhosis-precancerous lesion through regulating TGF-β1/Smad2/3 signal pathway, and provides experimental basis for prevention and cure of hepatic precancerous lesion of YiPiYangGanFang.