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Effects of mTOR on Neurological Deficits after Transient Global Ischemia

Jihong Xing1, Jian Lu2

  • 1Department of Emergency Medicine, The First Hospital of Jilin University, Changchun, Jilin 130021, China.

Translational Neuroscience
|July 22, 2017
PubMed

Insights

Blocking the mammalian target of rapamycin (mTOR) pathway reduces brain damage and neurological deficits after cardiac arrest. This mTOR inhibition lessens inflammation, apoptosis, and improves vascular endothelial growth factor (VEGF) levels in the hippocampus.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • The mammalian target of rapamycin (mTOR) pathway regulates crucial cellular processes like growth, proliferation, and survival.
  • Activation of mTOR signaling is implicated in various pathological conditions, including brain injury.

Purpose of the Study:

  • To investigate the role of the mTOR pathway in brain injuries and neurological deficits following transient global ischemia induced by cardiac arrest (CA).
  • To evaluate the therapeutic potential of blocking mTOR signaling using rapamycin in a rat model of CA-induced ischemia.

Main Methods:

  • Transient global ischemia was induced in rats via asphyxia followed by cardiopulmonary resuscitation (CPR).
  • Expression levels of p-mTOR, phosphorylated 4E-binding protein 4 (4E-BP1), and p70 ribosomal S6 protein kinase 1 (S6K1) were assessed.
  • The effects of rapamycin treatment on pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), Caspase-3, vascular endothelial growth factor (VEGF), and its receptor VEGFR-2 were analyzed.
  • Neurological deficits and brain water content were evaluated.

Main Results:

  • mTOR pathway activation (increased p-mTOR, p-4E-BP1, p-S6K1) was observed in rats subjected to CA.
  • Rapamycin treatment attenuated the upregulation of pro-inflammatory cytokines and Caspase-3, indicating reduced inflammation and apoptosis.
  • Blocking mTOR with rapamycin promoted VEGF and VEGFR-2 levels in the hippocampus.
  • Rapamycin administration led to improved neurological function and reduced brain water content in CA rats.

Conclusions:

  • Activation of the mTOR signaling pathway contributes to the pathophysiology of CA-induced transient global ischemia.
  • Inhibition of the mTOR pathway with rapamycin demonstrates neuroprotective effects.
  • Targeting mTOR signaling pathways offers a promising therapeutic strategy for mitigating neural dysfunction and vulnerability associated with transient global ischemia.
Keywords:
Caspase-3cardiac arrestcardiopulmonary resuscitationcytokineshippocampusmTORrapamycin

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