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PDK4 Decrease Neuronal Apoptosis via Inhibiting ROS-ASK1/P38 Pathway in Early Brain Injury After Subarachnoid

Xuan Gao1, Yong-Yue Gao1, Hui-Ying Yan1

  • 1Department of Neurosurgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China.

Antioxidants & Redox Signaling
|September 9, 2021
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Summary

Early brain injury after subarachnoid hemorrhage involves metabolic disorders. Pyruvate dehydrogenase kinase 4 (PDK4) overexpression reduces oxidative stress and neuronal apoptosis via the ROS/ASK1/P38 pathway, suggesting PDK4 as a therapeutic target.

Keywords:
PDHPDK4ROSSAHneuronal apoptosisoxidative stress

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Area of Science:

  • Neuroscience
  • Metabolic Disorders
  • Oxidative Stress

Background:

  • Metabolic disorders contribute to oxidative stress and neuronal apoptosis in early brain injury (EBI) post-subarachnoid hemorrhage (SAH).
  • Pyruvate dehydrogenase (PDH) activity decreases in EBI after SAH, linked to oxidative stress.
  • Pyruvate dehydrogenase kinase 4 (PDK4) is notably upregulated after SAH among PDK isozymes.

Purpose of the Study:

  • To investigate the role and mechanisms of PDK4 in oxidative stress following SAH.
  • To explore the therapeutic potential of targeting the PDK4-PDH axis in EBI.

Main Methods:

  • Utilized small interfering RNA (siRNA) to reduce PDK4 expression.
  • Employed a lentiviral vector for PDK4 overexpression.
  • Administered dichloroacetic acid (DCA) to modulate PDK4 activity.
  • Assessed PDH phosphorylation and activity, reactive oxygen species (ROS) production, and the ASK1/P38 pathway activation.

Main Results:

  • PDK4 overexpression inhibited PDH activity and altered cellular metabolism.
  • siRNA-mediated PDK4 knockdown increased ROS, activated the ASK1/P38 pathway, and induced apoptosis.
  • Lentiviral PDK4 overexpression attenuated PDH activity, oxidative stress, and neuronal apoptosis.
  • DCA inhibited PDK4 activity but induced feedback-driven PDK4 expression, leading to increased ROS and apoptosis.

Conclusions:

  • The PDK4-PDH axis exhibits antioxidant and antiapoptotic effects in EBI after SAH.
  • Early PDK4 overexpression mitigates neuronal apoptosis by reducing oxidative stress through the ROS/ASK1/P38 pathway.
  • PDK4 represents a potential therapeutic target for ameliorating EBI post-SAH.