Mounting evidence suggests that long non-coding RNAs (lncRNAs) and
microRNAs exert a critical regulatory role in
acute pancreatitis. The present study aimed to explore the role of
lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in
acute pancreatitis (AP) that was induced by
caerulein in rat pancreatic acinar cells (AR42J). The potential target sites of
lncRNA NEAT1 and miR-365a-3p were predicted using starBase and were confirmed using dual-
luciferase reporter assay. Reverse transcription-quantitative polymerase chain reaction was performed to assess
lncRNA NEAT1 and miR-365a-3p expression levels in AP induced by
caerulein. Cell Counting Kit-8 and flow cytometry assays were performed to assess AR42J cell viability. Western blotting was performed to evaluate the expression of apoptosis-related
proteins.
Interleukin (IL)-1β,
IL-6, and
tumor necrosis factor-α levels were detected by ELISA. The results of the dual-
luciferase reporter assay confirmed that miR-365a-3p could bind to NEAT1.
LncRNA NEAT1 was upregulated in AR42J cells treated with 10 nmol/l
caerulein, and miR-365a-3p was expressed at low levels in an AP model. Overexpression of miR-365a-3p suppressed the apoptosis and inflammatory response of AR42J cells induced by
caerulein. Importantly, inhibition of
lncRNA NEAT1 decreased apoptosis and
inflammation in
caerulein-treated AR42J cells, while these effects were reverted upon co-transfection with a miR-365a-3p inhibitor. In conclusion,
lncRNA NEAT1 was involved in AP progression by sponging miR-365a-3p and may thus be a novel target for treating patients with AP.