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.

中文翻译：

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MicroRNA-532-5p 通过下调 CCND1 的表达水平来调节高糖诱导的胰腺 β 细胞的氧化应激和胰岛素分泌损伤。

糖尿病是一种由胰岛素分泌不足引起的代谢紊乱。microRNA (miR)‑532‑5P 在糖尿病中的表达下调，但其在糖尿病中的具体作用尚未阐明。本研究旨在探讨 miR-532-5p 对糖尿病影响的具体机制。使用 MTT 测定法确定细胞活力。使用逆转录定量 PCR 检测 miR‑532‑5P、cyclin D1 (CCND1)、Insulin1 和 Insulin2 的表达水平。通过细胞转染，miR-532-5p 和 CCND1 的表达在细胞中过表达。ELISA用于检测胰岛素分泌。2',7'-二氯二氢荧光素二乙酸酯用于量化细胞中的活性氧水平。使用 TUNEL 测定法检测细胞凋亡。进行蛋白质印迹以检测凋亡相关蛋白CCND1和p53的表达。进行了双荧光素酶报告基因检测，验证了 miR‑532‑5p 和 CCND1 的靶向结合。miR-532-5p 的表达在高糖 (HG) 诱导的 MIN6 细胞中下调。miR-532-5p的过表达可以改善HG诱导的胰岛素分泌下降，抑制HG诱导的细胞氧化应激和细胞凋亡。miR‑532‑5p 可以靶向和调节 CCND1 的表达。miR-532-5p 的过表达通过下调参与调节 p53 表达的 CCND1 来下调 HG 诱导的细胞胰岛素分泌、氧化应激和细胞凋亡。总之，miR-532-5p 通过下调 CCND1 的表达来调节 HG 诱导的胰腺 β 细胞中的氧化应激和胰岛素分泌损伤，