肝细胞癌放射治疗后肝功能损害是制约肝癌放疗应用的瓶颈。肝再生有助于肝功能恢复，其在肝部分切除和ALPPS等得到广泛研究，然而放射治疗后肝细胞再生相关研究及机制鲜有报道。.课题组前期发现Akt、mTOR基因mRNA高表达于肝癌放疗后肝细胞再生组织中；细胞体外实验mTOR抑制剂降低放疗后正常肝细胞株的克隆形成能力。因此我们提出假说：Akt-mTOR信号通路调控肝脏放疗后的肝细胞再生。.为验证此假说，拟建立大鼠肝右叶大分割放疗-肝左叶再生的动物模型，应用Akt-mTOR信号通路抑制剂（Akt inhibitor，mTOR inhibitor）和通路激动剂（卡马西平）干预放疗-肝再生动物模型；通过RT-PCR和Western Blot等实验技术，在mRNA、总蛋白水平及磷酸化水平，探讨Akt-mTOR信号通路调控放疗后肝细胞再生的机制，为临床防治放射性肝功能损害和肝再生提供治疗靶点。

Liver function damage after radiotherapy for hepatocellular carcinoma (HCC) is the bottleneck restricting the application of radiotherapy for HCC. Liver regeneration contributes to the recovery of liver function, which has been extensively studied in partial hepatectomy and ALPPS, etc. However, the related studies and mechanisms of liver regeneration after radiotherapy have rarely been reported. .Our previous results found that mRNA of Akt and mTOR were significantly highly expressed in HCC patients with liver regeneration after radiotherapy comparing to those without regeneration after radiotherapy. It was also verified that mTOR inhibitor could reduce the clonal formation ability of liver normal cell lines after radiotherapy in vitro experiments. Therefore, we hypothesized that the Akt-mTOR signaling pathway might regulate liver regeneration after radiotherapy..We aim to establish an animal model of liver regeneration after liver fractionated irradiation in Sprague-Dawley rats. Animal models were treated with Akt-mTOR signaling pathway inhibitor (Akt inhibitor, mTOR inhibitor) and pathway agonist (carbamazepine) in vivo experiment. Using RT-PCR, Western Blot and other experimental techniques, the molecular mechanism of Akt-mTOR signaling pathway regulating liver regeneration after radiotherapy were investigated at mRNA, total protein and phosphorylation level. This study may provide therapeutic targets for clinical prevention and treatment of liver function damage and liver regeneration after radiation.