《中国肝癌诊治指南》已经推荐Ⅲ期患者接受放疗，放射性肝损伤（RILD）是继发于肝脏放疗的致死性并发症，制约放疗效果的提高。我科前期的研究已证实肝脏受辐射后非实质细胞释放的细胞因子提高肝实质细胞的放射敏感性，即RILD与其肝细胞所处的微环境有重要关系。我们拟通过生物信息学技术研究放疗后肝脏微环境的变化对肝细胞及乙肝病毒感染的肝细胞影响，以及它们在RILD发生发展中的相互作用及调控机制。期望能筛选出与肝细胞放射敏感性密切相关的蛋白，放疗后正常肝脏释放的细胞因子以及病毒感染的情况下释放细胞因子的差异，它们与肝细胞凋亡、肝脏损伤相关的信号传导通路，为今后预防、治疗放射性肝损伤提供有意义的"靶点"。

Radiotherapy (RT) is recommended as a treatment strategy for stage III hepatocellular carcinoma (HCC) by the Chinese Society of Liver Disease. Radiation-induced liver disease (RILD) is a fatal complication that restricts the therapeutic effect of RT. In a previous study, we showed that irradiated hepatic nonparenchymal cells release some cytokines that play an important role in sensitization of hepatic parenchymal cells. The hepatic microenvironment influences the radiation sensitivity of hepatic parenchymal cells. We established a protocol to study how changes in the microenvironment of irradiated liver may influence uninfected and hepatitis B virus (HBV)-infected hepatocytes. The design is such that it may be possible to elucidate factors playing key roles in RILD by bioinfomatic analysis. Major objectives will be identifying proteins closely associated with radiation sensitization of hepatic cells and determining differential cytokine profiles between post-irradiated uninfected versus HBV-infected liver. We will focus on the proteins or cytokines related to possible signal transduction pathways that may affect hepatocyte apoptosis or liver injury. With this approach, we hope to devise targeting strategies for RLID prevention or treatment.