Immunological response in early brain injury after SAH

Acta Neurochir Suppl. 2011;110(Pt 1):57-61. doi: 10.1007/978-3-7091-0353-1_10.

Abstract

This study summarized the role of inflammation in the early brain injury after subarachnoid hemorrhage. Elevation of cytokines, activation of MMPs and phosphorylation of MAPK contributes to neuronal apoptosis and brain edema. Anti-inflammation may be potential strategy for the prevention and suppression of early brain injury after subarachnoid hemorrhage.

Publication types

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

MeSH terms

  • Amino Acid Chloromethyl Ketones / therapeutic use
  • Animals
  • Brain Edema / etiology
  • Brain Edema / prevention & control
  • Brain Injuries / drug therapy
  • Brain Injuries / etiology*
  • Brain Injuries / immunology*
  • Cytokines / metabolism
  • Cytokines / therapeutic use
  • Encephalitis / etiology*
  • Encephalitis / metabolism
  • Encephalitis / prevention & control
  • Enzyme Inhibitors / therapeutic use
  • Gene Expression Regulation / drug effects
  • Humans
  • Matrix Metalloproteinase 9 / metabolism
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Subarachnoid Hemorrhage / complications*

Substances

  • Amino Acid Chloromethyl Ketones
  • Cytokines
  • Enzyme Inhibitors
  • N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone
  • Mitogen-Activated Protein Kinase Kinases
  • Matrix Metalloproteinase 9