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Inhibiting of GRASP65 Phosphorylation by DL-3-N-Butylphthalide Protects against Cerebral Ischemia-Reperfusion Injury

Bei-Lei Zhu1,2, Chen-Long Xie2, Ning-Ning Hu3

  • 1Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China.

Behavioural Neurology
|August 30, 2018
PubMed
Abstract

Insights

DL-3-n-butylphthalide (NBP) protects the brain from cerebral ischemia-reperfusion injury (CIRI) by inhibiting the ERK signaling pathway. This action reduces GRASP65 phosphorylation, offering a potential therapeutic strategy for brain injury.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Cerebral ischemia-reperfusion injury (CIRI) is a critical condition with significant neurological consequences.
  • The extracellular signal-regulated kinase (ERK) signaling pathway plays a role in the pathophysiology of CIRI.

Purpose of the Study:

  • To investigate the protective effects of DL-3-n-butylphthalide (NBP) against CIRI in a mouse model.
  • To elucidate the involvement of the ERK signaling pathway and GRASP65 phosphorylation in NBP's therapeutic action.

Main Methods:

  • A mouse model of CIRI was established using the Pulsinelli four-vessel occlusion method.
  • Mice were treated with NBP (90 mg/kg/d) either before or after reperfusion.
  • Infarction area, neurological severity, oxidative stress markers (SOD, MDA), and protein expressions (GRASP65, pGRASP65, ERK, pERK) were analyzed.

Main Results:

  • CIRI activated the ERK signaling pathway and increased GRASP65 phosphorylation.
  • NBP treatment significantly reduced infarct volume and neurological deficits.
  • NBP decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) levels.
  • NBP inhibited the activation of the ERK pathway and reduced GRASP65 phosphorylation.

Conclusions:

  • DL-3-n-butylphthalide (NBP) demonstrates neuroprotective effects against cerebral ischemia-reperfusion injury (CIRI).
  • NBP exerts its protective effects by inhibiting the ERK signaling pathway and subsequently reducing GRASP65 phosphorylation.
  • These findings suggest NBP as a potential therapeutic agent for treating CIRI.

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