This research was designed to ascertain the mechanism of miR-122-5p in alleviating the inflammation and fibrosis of acute pancreatitis (AP) mice.

Material and methods:
AP mouse or cell model was established by caerulein (CAE) treatment. The coefficient of pancreas was evaluated and the expression levels of amylase (AMS) and lipase were measured by kit. The pathological changes of pancreatic tissues were observed under hematoxylin-eosin (H&E) staining. The expression levels of fibrous proteins (α-SMA and Collagen Ⅰ) were detected. The expression levels of related inflammatory factors (IL-1β, IL-6, and TNF-α) were tested by ELISA. The correlations between miR-122-5p and HDAC1 or between HDAC1 and APOE were predicted and validated.

In AP mice or cells, the coefficient of pancreas was elevated (P < 0.01), and the AMS expression was increased (P < 0.001) while lipase expression was decreased (P < 0.05). The pathological structural change was obvious and the Rongione score was elevated (P < 0.001). The expression levels of α-SMA and Collagen Ⅰ were stimulated (P < 0.05), and the levels of IL-1β, IL-6, and TNF-α were enhanced (P < 0.001). miR-122-5p negatively regulated HDAC1 expression and HDAC1 inhibited APOE transcription. Overexpression of miR-122-5p or APOE could both reduce the inflammation and fibrosis in AP mice or cells but upregulation of HDAC1 or APOE inhibition reversed the inhibiting effect of miR-122-5p overexpression on CAE-induced inflammation and fibrosis.

Conclusively, miR-122-5p inhibited inflammation and fibrosis in an AP mouse model by the HDAC1/APOE axis.