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An In Vivo Assessment of Blood-Brain Barrier Disruption in a Rat Model of Ischemic Stroke
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Stanniocalcin-1 ameliorates cerebral ischemia by decrease oxidative stress and blood brain barrier permeability.

Sandra Bonfante1, Amanda Della Giustina1, Lucineia Gainski Danielski1

  • 1Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Graduate Program in Health Sciences, Health Sciences Unit, University of South Santa Catarina, Tubarão, SC, Brazil.

Microvascular Research
|November 17, 2019
PubMed
Summary

Stanniocalcin-1 (STC-1) protein reduces brain damage after ischemic stroke by lowering blood-brain barrier permeability and oxidative stress. This neuroprotective effect was observed in a rat model, highlighting STC-1

Keywords:
Blood brain barrierOxidative stressStanniocalcin-1Stroke

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathophysiology

Background:

  • Ischemic stroke causes brain damage via blood-brain barrier (BBB) disruption and oxidative stress.
  • Stanniocalcin-1 (STC-1) is a neuroprotective protein with known anti-inflammatory and anti-oxidative properties.

Purpose of the Study:

  • To investigate the therapeutic effects of STC-1 on BBB permeability and oxidative stress in a rat model of cerebral ischemia/reperfusion (I/R).

Main Methods:

  • Male Wistar rats underwent global cerebral I/R or sham procedures.
  • Intracerebroventricular administration of human recombinant STC-1 (100 ng/kg) or saline.
  • Neurological evaluation, brain water content, BBB permeability, nitrite/nitrate levels, lipid peroxidation, protein carbonyls, superoxide dismutase (SOD), and catalase (CAT) activity were assessed.

Main Results:

  • Cerebral I/R induced neurological deficits, increased brain water content, and elevated BBB permeability in multiple brain regions.
  • STC-1 administration significantly reduced BBB permeability and oxidative stress markers, including lipid peroxidation and protein carbonyls.
  • STC-1 reestablished reduced superoxide dismutase (SOD) and catalase (CAT) activities in specific brain regions.

Conclusions:

  • STC-1 demonstrates significant neuroprotective effects against cerebral I/R injury in rats.
  • These protective effects are mediated by the reduction of blood-brain barrier permeability and oxidative stress.
  • STC-1 represents a potential therapeutic agent for ischemic stroke treatment.