MicroRNA-532-5p regulates oxidative stress and insulin secretion damage in high glucose-induced pancreatic β cells by downregulating the expression levels of CCND1

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.