At present, there is no accurate method for evaluating the quality of liver transplant from a brain-dead donor. Proteomics are used to investigate the mechanisms involved in brain death‑induced liver injury and to identify sensitive biomarkers. In the present study, age‑ and gender‑matched rabbits were randomly divided into the brain death and sham groups. The sham served as the control. A brain‑death model was established using an intracranial progressive pressurized method. The differentially expressed proteins extracted from the liver tissues of rabbits that were brain‑dead for 6 h in the two groups were determined by two‑dimensional gel electrophoresis and matrix‑assisted laser desorption ionization time of flight mass spectrometry. Although there was no obvious functional and morphological difference in 2, 4 and 6 h after brain death, results of the proteomics analysis revealed 973±34 and 987±38 protein spots in the control and brain death groups, respectively. Ten proteins exhibited a ≥2‑fold alteration. The downregulated proteins were: aldehyde dehydrogenase, runt‑related transcription factor 1 (RUNX1), inorganic pyrophosphatase, glutamate‑cysteine ligase regulatory subunit and microsomal cytochrome B5. By contrast, the expression of dihydropyrimidinase-related protein 4, peroxiredoxin‑6, 3‑phosphoinositide‑dependent protein kinase‑1, 3-mercaptopyruvate and alcohol dehydrogenase were clearly upregulated. Immunohistochemistry and western blot analysis results revealed that the expression of RUNX1 was gradually increased in a time‑dependent manner in 2, 4, and 6 h after brain death. In conclusion, alteration of the liver protein expression profile induced by brain death indicated the occurrence of complex pathological changes even if no functional or morphological difference was identified. Thus, RUNX1 may be a sensitive predict factor for evaluating the quality of brain death donated liver.

Diabetes mellitus is a metabolic disorder caused by insufficient insulin secretion. The expression of microRNA (miR)-532-5P is downregulated in diabetes, but its specific role in diabetes has not yet been elucidated. The present study aimed to investigate the specific mechanism underlying the effects of miR-532-5p on diabetes. Cell viability was determined using an MTT assay. The expression levels of miR-532-5P, cyclin D1 (CCND1), Insulin1 and Insulin2 were detected using reverse transcription-quantitative PCR. The expression of miR-532-5p and CCND1 were overexpressed in cells by cell transfection. ELISA was used to detect insulin secretion. 2′,7′-dichlorodihydrofluorescein diacetate was used to quantify reactive oxygen species levels in cells. Apoptosis was detected using a TUNEL assay. Western blotting was performed to detect the expression of apoptosis-related proteins, CCND1 and p53. A dual-luciferase reporter assay was conducted, and verified the targeted binding of miR-532-5p and CCND1. The expression of miR-532-5p was downregulated in high glucose (HG)-induced MIN6 cells. Overexpression of miR-532-5p could improve the HG-induced decline in insulin secretion and inhibit HG-induced oxidative stress and apoptosis in cells. miR-532-5p can target and regulate the expression of CCND1. Overexpression of miR-532-5p downregulated HG-induced cell insulin secretion, oxidative stress and apoptosis by downregulating CCND1, which is involved in regulating the expression of p53. To conclude, miR-532-5p regulated oxidative stress and insulin secretion damage in HG-induced pancreatic β cells by downregulating the expression of CCND1, which is involved in the upregulation of the expression of p53.