Abstract: Objective To study the protective role of NR5A2 to acinar cells under acute pancreatitis. Methods Acute pancreatitis model was created by stimulating AR42J cells with cerulein. Virus vectors and shRNA were respectively used to upregulate or downregulate NR5A2 expression, and NR5A2 changes were verified by Western blot. Quantification of cell apoptosis was tested by flow cytometry. IL-1 and TNF-α expression were detected by ELISA. Results The apoptosis rate was significantly elevated under 100 nmol/L cerulein until the peak at 6 hours, meanwhile NR5A2 level was decreased until 24 h stimulation, and then gradually recovered to basal level after 48 h. NR5A2 overexpression further increased the apoptosis rate under cerulein stimulation (P<0.05), and reduced IL-1 and TNF-α levels (P<0.01, P<0.05). On the other hand, NR5A2 inhibition by shRNA led to decreased apoptosis rate (P<0.05) and increased IL-1 and TNF-α levels (P<0.05, P<0.01).Furthermore, silencing β-catenin attenuated the effects of NR5A2-overexpression, that the apoptosis rate was significantly reduced (P<0.05), while IL-1 and TNF-α levels were significantly increased (P<0.05, P<0.01). Conclusions NR5A2 induces apoptosis and inhibites inflammatory reaction in AR42J cells under cerulein stimulation, and such effects are mediated by β-catenin.

Key words: acute pancreatitis, cerulein, NR5A2, β-catenin, inflammatory factors