Background/Aims: Acute pancreatitis contributes to high mortality in pancreatitis patients, and miRNAs play a vital role in the development of acute pancreatitis (AP), however, its precise biological role remains largely elusive. Methods: To clarify the potential mechanisms of miRNAs in AP, we built mouse models of mild acute pancreatitis (MAP) and moderate/ severe acute pancreatitis (SAP). MiRNA microarray analysis and Real-time quantitative PCR (qRT-PCR) were used to analyze the expression of miRNA in MAP/SAP. TargetScan software, dual-luciferase gene reporter assays and Western blotting were used to assess the target genes of miR-155-5p in AP. Results: miR-155-5p was significantly decreased in MAP/SAP mice compared to controls. In pancreatic acinar AR42J cells transfected with miR-155-5p mimic, the expression of Rela and Traf3 notably decreased in both the caerulein- and TLC-S-induced groups compared with the negative control (NC); however, the expression of Rela and Traf3 notably increased after transfection with miR-155-5p inhibitor. Combined analysis using the TargetScan software and dual-luciferase gene reporter assays indicated that Rela and Traf3 were both targeted by miR-155-5p. Meanwhile, the expression of Ptgs2 also decreased after transfection of the AR42J cells with miR-155-5p mimic. The opposite results were found when miR-155-5p inhibitor was transfected into the AR42J cells. In addition, we treated caerulein- and TLC-S-induced AR42J cells with the Rela inhibitor helenalin and found that the expression of Rela, Traf3 and Ptgs2 decreased compared with the NC, while the expression of miR-155-5p did not show any significant difference. Furthermore, we found that miR-155-5p was significantly down-regulated in pancreatitis patients. Conclusion: miR-155-5p inversely regulated AP development through the Rela/Traf3/Ptgs2 signaling pathway.

Coronary heart disease (CHD) is the result of complex metabolic disorder caused by various environmental and genetic factors, and often comorbidity with anxiety. Anxiety was known to an independent risk factor for the adverse cardiovascular events and mortality in patients with CHD, while how stress-induced anxiety behavior impacts the metabolome of blood plasma in CHD patients and contributes to CHD worse is unclear. So this study aimed to investigate the effect of anxiety on metabolome of plasma in CHD patients. According to the inclusion and exclusion standard the blood plasma of CHD patients and CHD comorbidity with anxiety were collected after ethics approval. Metabolome analysis of blood plasma using liquid chromatography mass spectrometry (LC/MS) was performed, then multivariate data analysis was applied to evaluate the data. Disturbance of 39 plasma metabolites were altered in CHD patients accompany by anxiety patients as compared to control group. These disturbed metabolites were mainly involved in tryptophan metabolism, pyrimidine metabolism, glycerophospholipid metabolism, pentose phosphate metabolism, phenylalanine metabolism, pentose and glucuronate interconversions. The most significant pathway was tryptophan metabolism including the down-regulation of tryptophan and serotonin. In addition to tryptophan metabolism, the glycerophospholipids metabolism, pentose and glucuronate interconversions and pentose phosphate pathway were also greatly affected in this study. These results suggest that anxiety may further disturb CHD three translation of material metabolome. Besides theses metabolism pathway pyrimidine metabolism disturbed significantly which can aggravate the disease in patients with CHD. From these resoults the plasma metabolites monitoring was suggested to be recommended and may be conducive to early detect biomarkers to personalized treatment anxiety in patients with CHD in future.