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Updated: May 8, 2025

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction
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Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Published on: May 7, 2015

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CDC42 Regulates the ERK Pathway to Improve Oxygen‒Glucose Deprivation/Reoxygenation-Induced Neural Oxidative Stress

Lina Hao1, Hongmei Jia2, Feifei Wei3

  • 1Functional Department, CangZhou Hospital of Integrated TCM-WM HEBEI, Cangzhou, 061001, China.

Molecular Neurobiology
|March 4, 2025
PubMed

Insights

CDC42 overexpression reduces neural apoptosis and oxidative stress following oxygen-glucose deprivation/reoxygenation (OGD/R) by regulating the ERK pathway. This finding offers a potential therapeutic target for OGD/R-induced neural injury.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • CDC42 is known to regulate neural development and injury.
  • Its role in oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neural injury remains unexplored.
  • Oxidative stress and apoptosis are key features of OGD/R-induced neural damage.

Purpose of the Study:

  • To investigate the effect of CDC42 overexpression on neural injury and oxidative stress during OGD/R.
  • To elucidate the underlying molecular mechanisms involving the ERK pathway.

Main Methods:

  • Established an OGD/R cellular model using HT22 cells.
  • Utilized CDC42 overexpression vectors (oeCDC42) and an ERK inhibitor (PD98059).
  • Assessed cell viability, apoptosis, reactive oxygen species (ROS), superoxide dismutase (SOD) activity, and protein expression (p-ERK, p-c-Fos).

Main Results:

  • OGD/R induced time-dependent increases in neural apoptosis and ROS, and decreases in cell viability and SOD activity.
  • oeCDC42 significantly reduced apoptosis and ROS, and increased SOD activity in OGD/R-treated cells.
  • oeCDC42 upregulated p-ERK and p-c-Fos expression, while PD98059 reversed these protective effects.

Conclusions:

  • CDC42 overexpression ameliorates OGD/R-induced neural oxidative stress and apoptosis.
  • The protective effects of CDC42 are mediated through the regulation of the ERK signaling pathway.
  • CDC42 represents a potential therapeutic target for mitigating OGD/R-induced neural damage.
Keywords:
CDC42ERK pathwayNeural apoptosisNeural oxidative stressOxygen–glucose deprivation/reoxygenation

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