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.
Keywords: diabetic encephalopathy; microRNA‑130b; oxidative stress; phosphatase and tensin homolog; rat.