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The Blood-brain Barrier00:49

The Blood-brain Barrier

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Related Experiment Video

Updated: Jan 14, 2026

An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke
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Vascular recanalization exacerbates BBB permeability after ischemic stroke.

Rong-Fei Wang1,2,3, Jing Liu3, Chang-Hui Chen2

  • 1Guangzhou University of Chinese Medicine, Guangzhou, China.

Frontiers in Neurology
|October 17, 2025
PubMed
Summary

Vascular recanalization after ischemic stroke worsens blood-brain barrier leakage by affecting tight junctions and transcytosis. This highlights the need for new strategies to protect the brain barrier and reduce complications.

Keywords:
blood–brain barrierischemic strokerecanalizationtight junctionstranscytosis

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Area of Science:

  • Neuroscience
  • Cerebrovascular Diseases
  • Pathophysiology

Background:

  • Ischemic stroke disrupts the blood-brain barrier (BBB), increasing permeability and causing brain edema and hemorrhagic transformation.
  • These changes are exacerbated by blood flow recovery, but the impact of vascular recanalization on BBB integrity remains unclear.

Purpose of the Study:

  • To investigate the effect of vascular recanalization on blood-brain barrier integrity following ischemic stroke.
  • To analyze the mechanisms underlying BBB changes, focusing on tight junctions and transcytosis pathways.

Main Methods:

  • Mice underwent middle cerebral artery occlusion with either 60-minute reperfusion (recanalization group) or permanent occlusion (non-recanalization group).
  • Blood-brain barrier permeability was assessed using IgG and FITC-dextran leakage assays.
  • Expression of tight junction proteins (occludin, ZO-1) and transcytosis proteins (Caveolin-1, MFSD2a) was analyzed via western blot.

Main Results:

  • The recanalization group showed significantly increased BBB leakage compared to the non-recanalization group.
  • Reperfusion led to reduced expression of tight junction proteins occludin and ZO-1.
  • Ischemia and reperfusion altered the ratio of Caveolin-1/MFSD2a, indicating impaired transcytosis, particularly in the recanalization group.

Conclusions:

  • Vascular recanalization exacerbates blood-brain barrier disruption by impairing both paracellular and transcytosis pathways.
  • These findings suggest potential therapeutic targets for protecting BBB integrity and reducing hemorrhagic transformation after stroke.