Severe acute pancreatitis (SAP) is characterized by persistent organ failure and a high mortality rate, early diagnosis and disease assessment are crucial for improving patient prognosis. To investigate the expression level, diagnostic value, and mechanism of action of serum miR-331-3p in patients with SAP. One hundred eighty-five patients with AP (including 130 patients with mild-to-moderate acute pancreatitis (MAP) and 55 patients with SAP) and 100 healthy controls (HC) were enrolled. RT-qPCR was conducted to detect the expression of serum miR-331-3p, and its diagnostic efficacy was analyzed using receiver operating characteristic (ROC) curves. Correlation analysis was carried out using the Pearson correlation coefficient. The molecular mechanism was explored by combining dual-luciferase reporter gene assay and cell function experiments. The level of serum miR-331-3p expression in the SAP group was markedly lower than that in the MAP and HC groups (P < 0.05). The AUC for distinguishing MAP from SAP was 0.866 (95% CI: 0.810–0.921), with a sensitivity of 83.6% and a specificity of 73.1%. miR-331-3p was strongly negatively correlated with SAP routine indicators, severity, and inflammation (P < 0.001). Mechanistically, miR-331-3p directly targets bromodomain protein 4 (BRD4), and the overexpression of miR-331-3p alleviate the inflammatory response in the SAP cell model and promote cell proliferation, whereas BRD4 overexpression reversed the effects of miR-331-3p. Serum miR-331-3p is notably downregulated in SAP and may attenuate pancreatic inflammation through BRD4 targeting and inhibition, proposing its candidacy as a diagnostic biomarker.
Xiong et al. (Fri,) studied this question.