MiR-21-3p aggravates injury in rats with acute hemorrhagic necrotizing pancreatitis by activating TRP signaling pathway.

To evaluate the expression and effect of miR-21-3p in pancreas and lung injury of acute hemorrhagic necrotizing pancreatitis (AHNP) rats. AHNP rat model was constructed via retrograde injection of 5% sodium taurocholate into biliary pancreatic duct. Then rats were divided into normal, sham, AHNP, mimics negative control (NC), miR-21-3p mimics, inhibitors NC, miR-21-3p inhibitors, miR-21-3p mimics + phosphate buffer saline and miR-21-3p mimics + Gd3+ groups (N = 10 in each group). The expression of miR-21-3p, TRP signaling pathway factor, apoptosis related protein and histology were studied in pancreatic and lung tissues. Apoptosis of pancreatic acinar cells was detected. Oxidative stress indexes were detected in lung tissues. The level of PaO2 and PaCO2 and the expression of amylase, lipase and inflammatory factors were detected in blood. Compared with normal and sham groups, the miR-21-3p expression was increased in pancreatic and lung tissues of AHNP rats. MiR-21-3p expression was successfully regulated. Down-regulated miR-21-3p promoted apoptosis of pancreatic acinar cells and restored its function in AHNP rats. Up-regulated miR-21-3p reduced the lung oxygenation function, promoted pathological damage, and aggravated oxidative stress injury in AHNP rats. Meanwhile, up-regulated miR-21-3p also promoted the expression of serum enzymes and inflammatory factors, and activated TRP signaling pathway in AHNP rats. And miR-21-3p aggravated pancreatitis and lung injury by activating transient receptor potential (TRP) signaling pathway in AHNP rats. miR-21-3p promoted the pancreatic injury, inhibited apoptosis of necrotic acinar cells and aggravated lung oxidative stress injury by activating TRP signaling pathway in AHNP rats.