IL-33 expression in the cerebral cortex following experimental subarachnoid hemorrhage in rats

Cell Mol Neurobiol. 2015 May;35(4):493-501. doi: 10.1007/s10571-014-0143-9. Epub 2014 Nov 23.

Abstract

Subarachnoid hemorrhage (SAH) is a pervasive and devastating condition in which inflammatory and apoptotic pathways contribute to poor outcome. Interleukin-33 (IL-33) plays a crucial role in the inflammatory and apoptotic pathways through binding of the transmembrane ST2 receptor. This study investigated the expression and cellular localization of IL-33 in the cerebral cortex after SAH in order to clarify the role of IL-33 after SAH. Sprague-Dawley rats were randomly divided into sham and SAH groups and evaluated 2, 6, and 12 h and 1, 2, 3, and 5 days after the surgery, with SAH animals subjected to prechiasmatic cistern SAH. IL-33 expression was measured by western blot analysis, real-time PCR, immunohistochemistry, and immunofluorescence. The mRNA levels of tumor necrosis factor (TNF)-α and IL-1β were also assessed. The expression of IL-33, IL-1β, and TNF-α was markedly elevated in the SAH as compared to the sham group; IL-33 was mainly localized in neurons and astrocytes and not microglia after SAH. Moreover, a significant positive association was observed between IL-33 and IL-1β expression. These findings indicate that IL-33 might play an important role in the inflammatory response following SAH.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / metabolism
  • Cell Nucleus / metabolism
  • Cerebral Cortex / metabolism*
  • Cerebral Cortex / pathology
  • Fluorescent Antibody Technique
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Interleukin-33 / genetics
  • Interleukin-33 / metabolism*
  • Male
  • Neurons / metabolism
  • Rats, Sprague-Dawley
  • Real-Time Polymerase Chain Reaction
  • Subarachnoid Hemorrhage / genetics
  • Subarachnoid Hemorrhage / metabolism*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Up-Regulation

Substances

  • Interleukin-1beta
  • Interleukin-33
  • Tumor Necrosis Factor-alpha