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Inhaled Methane Protects Rats Against Neurological Dysfunction Induced by Cerebral Ischemia and Reperfusion Injury:

Baocheng Zhang1, Mingqiang Gao2, Jie Shen1

  • 1Department of ICU, Jinshan Hospital afflitated to Fudan university, Shanghai, China.

Archives of Medical Research
|March 12, 2018
PubMed
Abstract

Insights

Methane inhalation significantly reduced neurological deficits and inflammation in rats with cerebral ischemia-reperfusion injury. This protective effect is mediated by the PI3K/Akt/HO-1 antioxidant pathway.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Cerebral ischemia-reperfusion (I/R) injury generates excessive reactive oxygen species (ROS), leading to neurological dysfunction and inflammation.
  • Understanding protective mechanisms against cerebral I/R injury is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the therapeutic potential of methane in mitigating cerebral I/R injury.
  • To elucidate the underlying molecular pathways, specifically the PI3K/Akt/HO-1 signaling cascade, involved in methane's protective effects.

Main Methods:

  • A rat model of cerebral I/R injury was established.
  • Rats inhaled a methane-air mixture during reperfusion.
  • Neurological deficits, oxidative stress markers (MDA), inflammatory cytokine (TNF-α), Akt phosphorylation, and HO-1 expression were assessed.
  • Inhibitors of HO-1, PI3K, and Akt were used to probe the signaling pathway.

Main Results:

  • Methane inhalation significantly attenuated neurological deficits in rats subjected to cerebral I/R.
  • Methane treatment markedly reduced elevated levels of MDA and TNF-α.
  • Methane administration led to increased Akt phosphorylation and HO-1 expression.
  • Inhibition of HO-1, PI3K, or Akt abolished the neuroprotective effects of methane.

Conclusions:

  • Methane demonstrates significant therapeutic potential for treating cerebral I/R injury.
  • The protective effects of methane are attributed to the activation of the PI3K/Akt/HO-1 antioxidant pathway.
Keywords:
Cerebral ischemia and reperfusion injuryHeme oxygenase-1MethanePI3K/Akt pathway

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