Objective:To investigate the mechanism of emodin protecting AR42J cells from injury based on JAK2/STAT3 singnaling pathway. MethodsAR42J cells were plated in 6-well plates at a concentration of 1×10,5, cells/mL, and divided into three groups: control group, cerulein group (cerulein 10-8 mol/L), and emodin groups (final concentration 0.25 mg/L, 0.5 mg/L and 1 mg/L). The iodine-starch colorimetric amylase (AMS) kit was used to determine the amylase activity level of the cell supernatant, and the sample collection time of cerulein stimulated AR42J cell model was determined; the TNF-α activity was detected by ELISA; and the JAK2/STAT3 pathway related protein expression was analysed by Western blot.  Results:①Compared with the control group, the levels of AMS, TNF-α, JAK2/STAT3 pathway related protein expression and other inflammatory indicators in the cerulein group significantly increased (P,<,0.05). ②Compared with cerulein group, in the emodin groups amylase activity, TNF-α content and relative mRNA expression of JAK2 and STAT3 in pancreatic acinar cell injury induced by cerulein reduced significantly (P,<,0.01). ③Emodin at the concentration of 0.5 mg/L and 1.0 mg/L had better invtervention effects than emodin at the concentration of 0.25 mg/L, and the difference was statistically significant (P,<,0.001).  Conclusion:Emodin can reduce the injury of pancreatic acinar cells induced by cerulein, and its mechanism may be related to the regulation of JAK2/STAT3 signaling pathway.