急性肝损伤可导致肝衰竭，病死率很高。我们前期分别在肝衰竭患者、三种急性肝损伤小鼠的肝组织和血清中；TNF-α、H2O2和血清饥饿诱导的肝细胞损伤模型以及LPS/Nigericin和LPS/ATP诱导的体外焦亡模型中发现肝细胞焦亡明显增多，且lncRNA-AIRN过表达；而敲低AIRN则抑制LPS/Nigericin诱导的肝细胞焦亡。此外，发现胸腺素β4（Tβ4）能够下调AIRN并抑制CCl4引起的肝细胞焦亡，明显减轻肝损伤。因此，提出Tβ4通过下调AIRN抑制肝细胞焦亡缓解急性肝损伤的假说。拟进一步在细胞和动物模型中探究AIRN与肝细胞焦亡及急性肝损伤的关系并阐明其作用机制；扩大样本检测AIRN在肝衰竭患者肝组织和血清中的水平，阐明其与肝衰竭发生及预后的关系；阐明Tβ4缓解急性肝损伤是通过抑制AIRN介导的肝细胞焦亡，为肝衰竭的防治提供新靶点。

The mortality of liver failure caused by severe acute liver injury is high. We found that hepatocyte pyroptosis was enhanced, together with over-expressed lncRNA-AIRN, in the liver tissue and serum of patients suffered from liver failure; in CCl4-, APAP- and D-gal/LPS- induced acute injured liver in mice; in TNF-α-, H2O2- and serum starvation-induced injured cells; in LPS/Nigericin- and LPS/ATP-induced pyroptotic hepatocytes, respectively. Moreover, knockdown of AIRN reduces LPS/Nigericin-induced hepatocyte pyroptosis. In addition, we found that treatment with Tβ4 reduced the level of AIRN and inhibited hepatocyte pyroptosis. Therefore, we hypothesize that Tβ4 down-regulates AIRN and subsequently reduces hepatocyte pyroptosis, alleviating acute liver injury. Further investigations will focus on the role and mechanism of AIRN and hepatocyte pyroptosis in the process of acute liver injury. Also, we will further detect the level of AIRN in liver and serum with enlarged patient samples, to elucidate the correlation of this molecule with the pathogenesis and prognosis of liver failure, illustrating that AIRN-mediated hepatocyte pyroptosis plays a role in Tβ4-alleviated acute liver injury, thus, confirming AIRN as a novel therapeutic target.