miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy

• Published in: International journal of molecular medicine Vol. 48; no. 1; p. 1
• Main Authors: Lei, Yonghua, Yang, Ming, Li, Hong, Xu, Rongjuan, Liu, Junbao
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications 01.07.2021; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Analysis; Apoptosis; Binding sites; Biotechnology; Biotechnology industry; Cardiovascular disease; Dextrose; Diabetes; Encephalopathy; Ethylenediaminetetraacetic acid; Experiments; Glucose; Life sciences; MicroRNA; MicroRNAs; Oxidative stress; Pathogenesis; Penicillin; Phosphatases; Proteins; Scientific equipment and supplies industry; Superoxide; United States; Japan; China
• ISSN: 1107-3756; 1791-244X
• DOI: 10.3892/ijmm.2021.4974

Diabetic encephalopathy (DE) is one of the main chronic complications of diabetes, and is characterized by cognitive defects. MicroRNAs (miRNAs/miRs) are widely involved in the development of diabetes-related complications. The present study evaluated the role of miR-130b in DE and investigated its mechanisms of action. PC12 cells and hippocampal cells were exposed to a high glucose environment to induce cell injuries to mimic the in vitro model of DE. Cells were transfected with miR-130b mimic, miR-130b inhibitor and small interfering RNA (si)-phosphatase and tensin homolog (PTEN) to evaluate the protective effect of the miR-130b/PTEN axis against oxidative stress in high glucose-stimulated cells involving Akt activity. Furthermore, the effect of agomir-130b was also assessed on rats with DE. The expression of miR-130b was reduced in the DE models in vivo and in vitro. The administration of miR-130b mimic increased the viability of high glucose-stimulated cells, prevented apoptosis, increased the activity of superoxide dismutase (SOD), decreased the malondialdehyde (MDA) content, activated Akt protein levels and inhibited the mitochondria-mediated apoptotic pathway. The administration of miR-130b inhibitor exerted opposite effects, while si-PTEN reversed the effects of miR-130b inhibitor. In vivo, the administration of agomir-130b attenuated cognitive disorders and neuronal damage, increased SOD activity, reduced the MDA content, activated Akt protein levels and inhibited the mitochondria-mediated apoptosis pathway in rats with DE. On the whole, these results suggest that miR-130b activates the PI3K/Akt signaling pathway to exert protective effects against oxidative stress injury via the regulation of PTEN in rats with DE.