TAB3 overexpression promotes NF-κB activation and inflammation in acute pancreatitis.

Acute pancreatitis (AP) is a clinically common inflammatory disease, NF-κB activation and the secretion of pro-inflammatory mediators have been considered as the main events of AP. According to reports, TAB3 is essential for NF-κB activation and participates in inflammatory responses. In this study, we used caerulein to establish an AP rat model and cell model. The expression of TAB3 was measured both in control group and AP group by Western blot and Immunohistochemistry. We firstly found the expression of TAB3 was significantly increased in caerulein-induced AP rat and cell model compared with control group, especially at 8 h. Furthermore, the increasing expression of TAB3 in AP group was also accompanied by increased levels of pro-inflammatory mediators (TNF-α, IL-6 and LDH). In addition, the decreasing expression of TAB3 in TAB3-siRNA transfected AP AR42J cells was accompanied by reduced levels of pro-inflammatory cytokines and inhibited the production of p-P65. These findings suggested that TAB3 may accelerate the inflammatory responses of AP through NF-κB activation.