Open Access

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

  • Authors:
    • Yonghua Lei
    • Ming Yang
    • Hong Li
    • Rongjuan Xu
    • Junbao Liu
  • View Affiliations

  • Published online on: May 31, 2021     https://doi.org/10.3892/ijmm.2021.4974
  • Article Number: 141
  • Copyright: © Lei et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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.
View Figures
View References

Related Articles

Journal Cover

July-2021
Volume 48 Issue 1

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Lei Y, Yang M, Li H, Xu R and Liu J: miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy. Int J Mol Med 48: 141, 2021
APA
Lei, Y., Yang, M., Li, H., Xu, R., & Liu, J. (2021). miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy. International Journal of Molecular Medicine, 48, 141. https://doi.org/10.3892/ijmm.2021.4974
MLA
Lei, Y., Yang, M., Li, H., Xu, R., Liu, J."miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy". International Journal of Molecular Medicine 48.1 (2021): 141.
Chicago
Lei, Y., Yang, M., Li, H., Xu, R., Liu, J."miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy". International Journal of Molecular Medicine 48, no. 1 (2021): 141. https://doi.org/10.3892/ijmm.2021.4974