Abstract： Objective： To explore the protective mechanism of triptolide against acute liver injury induced by carbon tetrachloride (CCl4) in rats based on nuclear factor E2 related factor 2/heme oxygenase/ quinone oxidoreductase 1 (Nrf2/HO-1/NQO1) signaling pathway. Methods： Forty SPF male SD rats were included and fed for seven days，and then were randomly divided into four groups (the normal group，the model group，the low-dose group and the high-dose group)，with 10 rats in each group. The normal group and the model group were injected with equal volume of 0.9% sodium chloride solution daily through the tail vein， and the low-dose group and the high-dose group were respectively injected with 100 mg/kg and 200 mg/kg triptolide for seven days. Three hours after the injection of triptolide on the seventh day (sterile saline in the model group)， rats in the model group， the low-dose group and the high-dose group were intraperitoneally injected with 1 mL/kg CCl4 to induce acute liver injury model (the normal group was intraperitoneally injected with equal volume of olive oil solution). Sixteen hours after CCl4 injection， the blood and liver samples of rats were collected， and the pathological changes of their liver sections were observed through HE histochemical staining， and the levels of serum liver function indexes， the protein levels and the mRNA expressions of Nrf2， HO-1 and NQO1 in liver tissues of the four groups were detected. Results：The histopathological examination showed that the liver cells in the normal group were arranged neatly， the structure and shape were normal， the cell boundaries were obvious， and that the cytoplasm was intact. In the model group，sixteen hours after CCl4 injection，the liver tissues showed the characteristics of hepatocyte necrosis such as unclear hepatocyte boundary and disordered cell arrangement， and the inflammatory cell infiltration and severe edema of hepatocytes showed bubble-like change. Compared with those in the model group，the degree of hepatocyte edema and the characteristics of hepatocyte necrosis in the low-dose and high-dose groups were lighter， and the degree in the highdose group was lighter than that in the low-dose group. The liver indexes in the model group， the lowdose group and the high-dose group were higher than those in the normal group， and the AST and ALT levels were higher than those in the normal group (P＜0.05)； the liver indexes in the model group were higher than those in the low-dose group and the high-dose group，and the indexes in the low-dose group were higher than those in the high-dose group (P＜0.05)；the AST and ALT levels in the model group were higher than those in the low-dose and the high-dose groups，and the levels in the low-dose group were higher than those in the high-dose group (P＜0.05). The protein levels and mRNA expressions of Nrf2， HO-1 and NQO1 in liver tissues of the model group，the low-dose group and the high-dose group were higher than those in the normal group；the above levels in the model group were higher than those in the low-dose group and the high-dose group，and the above levels in the low-dose group were higher than those in the high-dose group (P＜0.05). Conclusion：Triptolide can alleviate CCl4-induced acute liver injury in rats，and its mechanism may be related to the activation of Nrf2/HO-1/NQO1 signaling pathway to inhibit oxidative damage of hepatocytes.