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.