肝癌是临床上最常见的恶性肿瘤之一，介入治疗肝癌患者已有了广泛的应用，但患者在介入手术后会出现不同程度的肝功能下降，甚至肝衰竭。前期研究发现，肝癌介入治疗后，癌旁正常肝组织中炎性细胞、凋亡细胞明显增加，表明介入治疗对正常肝细胞有一定的损伤。PPAR-a、炎性反应、脂肪代谢异常以及缺血再灌注损伤之间有密切的关系。本实验建立SOD1,SOD2,SOD3高表达及基因敲除肝癌模型、兔肝癌TAE模型，以上模型进行WY14643、CMC预处理，检测SODs、NF-κB、MMP9的表达，构建含基因SODs、MMP9启动子序列的荧光素酶报告质粒，研究PPAR-α调控SOD1、SOD2、SOD3以及抑制MMP9的相关机制。本项目从研究PPAR-α改善TAE治疗后肝细胞氧化应激反应以及调控SODs、MMP9的机制入手，来研究PPAR-α改善TAE治疗后肝功能损伤的作用及其机制，为临床保护肝功能提供实验依据。

Primary liver cancer is one of the most common clinical malignant tumors，interventional treatment of liver cancer patients has been widely used.In recent years, we found that patients after intervention operation will be varying degrees of decreased liver function, and even liver failure.Our previous studies found that inflammatory cells, apoptotic cells was significantly increased in the adjacent liver cells after liver cancer interventional therapy, show that intervention has some damage on normal liver cells. PPAR-α is closely related with tumor,inflammatory response, abnormal fat metabolism and ischemia-reperfusion injury. In this study, the establishment of SOD1, SOD2, SOD3 high expression and gene knock liver cancer model, rabbit liver cancer model after TAE, the above models with WY14643, CMC pretreatment, detect expression of SODs、NF-κB、MMP9, construction of gene-containing SODs, MMP9 promoter sequence luciferase reporter plasmid, research the mechanisms of PPAR α regulation of SOD1, SOD2, SOD3 and inhibition of MMP9.This project research the mechanism of PPAR α improve oxidative stress in liver cell after TAE treatment and regulation SODs, MMP9,to study the effect that PPAR α improve liver function after TAE treatment and its mechanism，to provide experimental evidence for clinical protection of liver function.