• Complete inhibition of phosphatase and tensin homolog promotes the normal and oxygen-glucose deprivation/reperfusion-injured PC12 cells to cell death
  • sohrab minaei beyrami,1,* Mohammad Hasan Khadem Ansari,2 Yousef Rasmi,3 Nader Shakib,4
    1. Department of Biochemistry and Clinical Laboratories, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
    2. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
    3. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
    4. Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran


  • Introduction: PTEN antagonizes PI3K/AKT cell survival pathway. The effect of PTEN inhibitors has been rarely examined on cell survival following reperfusion injury. We investigated the neuroprotective effect of SF1670, as a new PTEN inhibitor, on an in vitro stroke-like model.
  • Methods: PC12 cells were exposed to OGD/R. The cells were treated in five conditions as follows: NO/NG; 60 minutes OGD; 60 minutes OGD and 6 h reperfusion; OGD/R treated with 10 µM SF1670, and NO/NG treated with 10 µM SF1670. Phosphorylation levels of AKT, P38 in PC12 cells were measured by immunoblotting. The cell viability was also determined by colorimetric assay.
  • Results: The results of the current study showed that SF1670 increased p-AKT, and decreased p-P38, p-JNK, and cell viability in the PC12 cells exposed to OGD/R insult. This paper demonstrated that complete inhibition of phosphatase activity of PTEN promoted cells toward death, possibly through attenuation P38 signaling pathways in OGD/R PC12 cells.
  • Conclusion: Overall, our results demonstrated that complete inhibition of phosphatase activity of PTEN not only did not exhibit neuroprotective effect but also promoted PC12-deprived cells to death.
  • Keywords: OGD, Reperfusion Injury, AKT, P38, MAPK, PC12 Cells