肝纤维化是慢性肝病发展到肝硬化、肝癌的必经阶段，终末期肝硬化患者的致死率极高，延缓肝纤维化或肝硬化代偿阶段向失代偿阶段发展是控制肝病恶化的有效途径。但目前还未上市针对性治疗肝纤维化的药物，新药物的开发迫在眉睫。我们前期研究发现，来源于中药赤芍的降八碳达玛烷类化合物7C能够抑制肝星状细胞的增殖和活化，明显改善BDL诱导的大鼠肝纤维化，并且化合物7C能够降低肝星状细胞中羧酸酯酶1（CES1）的表达。本项目拟在此原创性基础上，以化合物7C降低CES1的表达为依据，通过体外过表达、肝硬化组织芯片、基因敲除小鼠等手段深入研究CES1在肝纤维化发生发展中的作用，同时阐明化合物7C调控CES1表达的分子机制。最终验证化合物7C通过下调CES1的表达，抑制肝星状细胞的活化，从而发挥其抗肝纤维化作用的假说。

Hepatic fibrosis is a necessary stage for the development of chronic liver disease to cirrhosis and hepatocellular carcinoma. The mortality rate of end-stage cirrhosis is extremely high, and delaying the development of hepatic fibrosis or compensated-stage cirrhosis to decompensate is an effective way to control liver disease. However, no specific anti-hepatic fibrosis drugs have appeared yet and to develop new drugs is urgent. Our previous study found that octanordammarane 7C that derived from the Chinese herb Radix Paeoniae Rubra can inhibit the proliferation and activation of hepatic stellate cells, and it can also improve the fibrosis induced by BDL in rats significantly. At the same time, we found that the expression of carboxylesterase 1 (CES1) in hepatic stellate cells was reduced by 7C. Based on this originality and according to the reduction effect of compound 7C on CES1, we would explore the role of CES1 in the development of hepatic fibrosis by in vitro overexpression, hepatic cirrhosis tissue microarray and knockout mice. At the same time, to elucidate the mechanism of compound 7C regulation on CES1 expression. Finally, we aim at to prove our hypothesis that compound 7C inhibits the activation of hepatic stellate cells and exerts its anti-hepatic fibrosis effect through repressing the expression of CES1.