The Role of Platelet-Derived Growth Factor Receptor in Early Brain Injury Following Subarachnoid Hemorrhage

J Stroke Cerebrovasc Dis. 2016 Sep;25(9):2203-8. doi: 10.1016/j.jstrokecerebrovasdis.2016.03.025. Epub 2016 Jul 7.

Abstract

Objective: This study aims to observe encephaledema and cell apoptosis in rats following subarachnoid hemorrhage (SAH) and to explore the mechanism of platelet-derived growth factor receptor (PDGFR) in the development of early brain injury (EBI).

Methods: Adult and male Sprague-Dawley rats were randomly divided into 4 groups: sham operation, SAH, SAH + imatinib, and SAH + platelet-derived growth factor-BB (PDGF-BB). SAH model was established using intravascular silk puncture of the internal carotid artery crotch. The SAH + imatinib group was treated with intraperitoneal injection of imatinib 1 hour before establishing the model. The SAH + PDGF-BB group was administered with intracerebroventricular injection of PDGF-BB 1 hour before establishing the model. The mortality, encephaledema, and nerve functional scoring were observed after 24 hours in all groups. The expression of caspase-3 in hippocampus was tested by reverse transcription polymerase chain reaction and Western blotting.

Results: Mortality and encephaledema were the highest in the SAH + PDGF-BB group, which were alleviated when the rats were injected with imatinib (P < .01).

Conclusion: PDGFR may participate in the pathogenesis of EBI following SAH. The antagonist of PDGFR, imatinib, can reduce brain damage to some degree.

Keywords: PDGFR; SAH; apoptosis; early brain injury; encephaledema.

MeSH terms

  • Animals
  • Anthracenes / therapeutic use
  • Antineoplastic Agents / therapeutic use
  • Brain Edema / etiology
  • Brain Injuries / etiology*
  • Brain Injuries / mortality
  • Brain Injuries / prevention & control
  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Disease Models, Animal
  • Double-Blind Method
  • Enzyme Inhibitors / therapeutic use
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology*
  • Hippocampus / metabolism*
  • Imatinib Mesylate / therapeutic use
  • In Situ Nick-End Labeling
  • Male
  • Platelet-Derived Growth Factor / therapeutic use
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Platelet-Derived Growth Factor / metabolism*
  • Subarachnoid Hemorrhage / complications*
  • Subarachnoid Hemorrhage / drug therapy

Substances

  • Anthracenes
  • Antineoplastic Agents
  • Enzyme Inhibitors
  • Platelet-Derived Growth Factor
  • RNA, Messenger
  • pyrazolanthrone
  • Imatinib Mesylate
  • Receptors, Platelet-Derived Growth Factor
  • Caspase 3