In the current study, TCA induces NF-κB upregulation and translocation to the nucleus in pancreatic acinar cells in both a dose- and time- dependent manner, and these effects were blocked by both JTE-013 (an antagonist of S1PR2) or S1PR2-shRNA, which further showed that S1PR2 activation was responsible for inflammation within acinar cells during the early phase of pancreatitis. Here, NFKB1 is linked to pancreatitis.