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Pyruvate kinase M2 (PKM2) improve symptoms of post-ischemic stroke depression by activating VEGF to mediate the

Yun Feng1, Xuebin Li2, Jie Wang3

  • 1Department of Neurology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise City, Guangxi Province, China.

Brain and Behavior
|December 13, 2021
PubMed
Abstract

Insights

Pyruvate kinase M2 (PKM2) alleviates post-stroke depression in rats by reducing inflammation and oxidative stress. This occurs through the activation of the VEGF-mediated MAPK/ERK pathway, improving depressive behaviors.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Post-stroke depression (PSD) is a common complication following ischemic stroke.
  • The underlying mechanisms of PSD are complex and not fully understood.
  • Pyruvate kinase M2 (PKM2) is implicated in various cellular processes, including inflammation and cell proliferation.

Purpose of the Study:

  • To investigate the effects of pyruvate kinase M2 (PKM2) on stroke-induced post-stroke depression (PSD) in a rat model.
  • To explore the underlying mechanisms by which PKM2 influences PSD, including its anti-inflammatory and anti-oxidative stress properties.
  • To determine the role of the VEGF/MAPK/ERK pathway in PKM2's therapeutic effects on PSD.

Main Methods:

  • Rats were induced with stroke and divided into groups receiving saline, recombinant PKM2 (rPKM2), or rPKM2 with bevacizumab.
  • Behavioral tests (sucrose preference, immobility, movement) were conducted to assess depressive symptoms.
  • Oligodendrocyte proliferation, inflammatory markers (TNF-α, IL-6, IL-1β), oxidative stress markers (MDA, LDH, NO), and pathway proteins (VEGF, PKM2, ERK) were analyzed using western blot, immunofluorescence, qPCR, and ELISA.

Main Results:

  • PKM2 administration significantly improved depressive behaviors in PSD rats.
  • PKM2 demonstrated anti-inflammatory and anti-oxidative stress effects, reducing key inflammatory and oxidative markers.
  • PKM2 treatment led to increased oligodendrocyte proliferation and activated the VEGF/MAPK/ERK signaling pathway.

Conclusions:

  • PKM2 effectively ameliorates depressive symptoms associated with post-stroke depression.
  • The therapeutic benefits of PKM2 in PSD are mediated by its anti-inflammatory and anti-oxidative stress actions.
  • PKM2 exerts its effects, at least in part, by activating the VEGF-mediated MAPK/ERK pathway.
Keywords:
ERKMAPKPKM2PSDVEGF

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