The pivotal role and mechanism of long non-coding RNA B3GALT5-AS1 in the diagnosis of acute pancreatitis.

The present study planned to dig the potential impacts of long non-coding RNA B3GALT5-AS1 in acute pancreatitis (AP). A total of 66 patients who were diagnosed with AP using ultrasonic imaging were enrolled in the study. Expression levels of B3GALT5-AS1 in the serum of AP patients were determined. Afterwards, rat pancreatic AR42J acinar cells were disposed with caerulein to produce AP-like injury. The role and molecular mechanisms of B3GALT5-AS1 in AP were explored through in vitro cell experiments. The levels of lncRNA B3GALT5-AS1 were observed to be lessened in patients with AP relative to healthy controls. In addition, caerulein was observed to induce injuries in the AR42J cells (depressed cell viability, enhanced cell apoptosis, cytokines production, and levels of amylase). Overexpression of B3GALT5-AS1 alleviated the caerulein-produced injury in the AR42J cells. Moreover, it was determined that miR-203 showed a downside expression by B3GALT5-AS1 regulation, and the overexpression of B3GALT5-AS1 retrained caerulein-produced injury through the suppression of miR-203. In addition, it was observed that miR-203 lessened the level of nuclear factor interleukin-3 (NFIL3) and that NFIL3 was targeted by miR-203. Lastly, the impacts of B3GALT5-AS1 on caerulein-induced cell injury were manifested through the NF-κB signalling pathway. The data from the present study revealed that in patients with AP, B3GALT5-AS1 is expressed in reduced amounts. Overexpression of B3GALT5-AS1 may alleviate caerulein-induced cell injury in AR42J cells through the regulation of miR-203/NFIL3 axis and by inhibiting the activation of the NF-κB signals.

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