Carbon tetrachloride (CCl4)-induced acute liver injury (ALI) rat model was used to evaluate the effects of PSPJ on liver histopathological changes by observing the general condition and body weight changes of rats, and the improvement of liver histopathological changes by hematoxylin-eosin staining (HE); the effects of PSPJ on liver histopathological changes were evaluated by observing the general condition and body weight changes of rats, and the improvement of liver histopathological changes by hematoxylin-eosin staining (HE). PSPJ) were administered to rats, and the ameliorative effect of PSPJ on the pathological changes of liver tissue was evaluated by observing the general condition and body weight changes of rats, using hematoxylin-eosin staining (HE); immunohistochemistry (IHC) staining to detect the expression of NF-κB in liver tissues; and protein immunoblotting (WB) and other methods to detect the effect of PSPJ on hepatic PI3K/AKT/ NF-κBR signaling pathway-related proteins and expression levels of inflammatory indicators. The results showed that the body weight, liver weight and liver index of the model group increased significantly (P<0.05); a large amount of inflammatory infiltration of liver tissue appeared in the model group, and the pathological changes of the liver in the drug group were obviously alleviated; compared with the normal group, p-PI3K protein expression in the liver tissue of the model group decreased significantly (P<0.05), and the expression of P I3K, p-AKT, p-NF-κB and IL-1β protein increased significantly (P<0.05); in the drug group, the expression of p-PI3K protein increased significantly (P<0.05), and that of p-AKT and IL-1β decreased significantly (P<0.05). In the drug group, p-PI3K protein expression was significantly increased (P<0.05), and p-AKT and IL-1β protein expression was significantly decreased (P<0.05). pSPJ could alleviate CCL4-induced acute liver injury through the expression of key proteins in the signaling of PI3K/AKT/NF-κB pathway in rats.