Hyperbaric oxygen preconditioning attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats

Exp Neurol. 2013 Sep:247:737-43. doi: 10.1016/j.expneurol.2013.03.019. Epub 2013 Mar 26.

Abstract

Hyperglycemia dramatically aggravates brain infarct and hemorrhagic transformation (HT) after ischemic stroke. Oxidative stress and matrix metalloproteinases (MMPs) play an important role in the pathophysiology of HT. Hyperbaric oxygen preconditioning (HBO-PC) has been proved to decrease oxidative stress and has been demonstrated to be neuroprotective in experimental stroke models. The present study determined whether HBO-PC would ameliorate HT by a pre-ischemic increase of reactive oxygen species (ROS) generation, and a suppression of MMP-2 and MMP-9 in hyperglycemic middle cerebral artery occlusion (MCAO) rats. Rats were pretreated with HBO (100% O₂, 2.5 atmosphere absolutes) 1 h daily for 5 days before MCAO. Acute hyperglycemia was induced by an injection of 50% dextrose. Neurological deficits, infarction volume and hemorrhagic volume were assessed 24 h and 7 days after ischemia. ROS scavenger n-acetyl cysteine (NAC), hypoxia-inducible factor-1α (HIF-1α), inhibitor 2-methoxyestradiol (2ME2) and activator cobalt chloride (CoCl₂), and MMP inhibitor SB-3CT were administrated for mechanism study. The activity of MMP-2 and MMP-9, and the expression HIF-1α were measured. HBO-PC improved neurological deficits, and reduced hemorrhagic volume; the expression of HIF-1α was significantly decreased, and the activity of MMP-2 and MMP-9 was reduced by HBO-PC compared with vehicle group. Our results suggested that HBO-PC attenuated HT via decreasing HIF-1α and its downstream MMP-2 and MMP-9 in hyperglycemic MCAO rats.

Keywords: Hemorrhagic transformation; Hyperbaric oxygen preconditioning; MCAO; MMP-2 and MMP-9.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Analysis of Variance
  • Animals
  • Blood Glucose
  • Cerebral Hemorrhage / etiology*
  • Cerebral Hemorrhage / prevention & control*
  • Cerebral Infarction / etiology
  • Cerebral Infarction / prevention & control
  • Cobalt / pharmacology
  • Disease Models, Animal
  • Free Radical Scavengers / therapeutic use
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology
  • Glucose / toxicity
  • Hemoglobins / metabolism
  • Hyperbaric Oxygenation / methods*
  • Hyperglycemia / chemically induced
  • Hyperglycemia / complications*
  • Infarction, Middle Cerebral Artery / complications*
  • Ischemic Preconditioning / methods*
  • Male
  • Metalloproteases / metabolism*
  • Neurologic Examination
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism
  • Spectrophotometry
  • Time Factors

Substances

  • Blood Glucose
  • Free Radical Scavengers
  • Hemoglobins
  • Reactive Oxygen Species
  • Cobalt
  • Metalloproteases
  • cobaltous chloride
  • Glucose