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

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.

Automated summary

The study revealed that miR-130b is downregulated in diabetic encephalopathy, and exerts a protective effect against oxidative stress injury by activating the PI3K/Akt signaling pathway through regulating PTEN.