Astaxanthin offers neuroprotection and reduces neuroinflammation in experimental subarachnoid hemorrhage

J Surg Res. 2014 Nov;192(1):206-13. doi: 10.1016/j.jss.2014.05.029. Epub 2014 May 21.

Abstract

Background: Neuroinflammation has been proven to play a crucial role in early brain injury pathogenesis and represents a target for treatment of subarachnoid hemorrhage (SAH). Astaxanthin (ATX), a dietary carotenoid, has been shown to have powerful anti-inflammation property in various models of tissue injury. However, the potential effects of ATX on neuroinflammation in SAH remain uninvestigated. The goal of this study was to investigate the protective effects of ATX on neuroinflammation in a rat prechiasmatic cistern SAH model.

Methods: Rats were randomly distributed into multiple groups undergoing the sham surgery or SAH procedures, and ATX (25 mg/kg or 75 mg/kg) or equal volume of vehicle was given by oral gavage at 30 min after SAH. All rats were sacrificed at 24 h after SAH. Neurologic scores, brain water content, blood-brain barrier permeability, and neuronal cell death were examined. Brain inflammation was evaluated by means of expression changes in myeloperoxidase, cytokines (interleukin-1β, tumor necrosis factor-α), adhesion molecules (intercellular adhesion molecule-1), and nuclear factor kappa B DNA-binding activity.

Results: Our data indicated that post-SAH treatment with high dose of ATX could significantly downregulate the increased nuclear factor kappa B activity and the expression of inflammatory cytokines and intercellular adhesion molecule-1 in both messenger RNA transcription and protein synthesis. Moreover, these beneficial effects lead to the amelioration of the secondary brain injury cascades including cerebral edema, blood-brain barrier disruption, neurological dysfunction, and neuronal degeneration.

Conclusions: These results indicate that ATX treatment is neuroprotective against SAH, possibly through suppression of cerebral inflammation.

Keywords: Astaxanthin; Early brain injury; Inflammation; Subarachnoid hemorrhage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood-Brain Barrier / drug effects
  • Brain Edema / drug therapy
  • Brain Edema / immunology
  • Brain Edema / metabolism
  • Cell Death / drug effects
  • Disease Models, Animal
  • Interleukin-1beta / metabolism
  • Male
  • NF-kappa B / metabolism
  • Neuritis / drug therapy*
  • Neuritis / immunology
  • Neuritis / metabolism
  • Neuroprotective Agents / pharmacology*
  • Optic Chiasm / drug effects
  • Optic Chiasm / immunology
  • Optic Chiasm / metabolism
  • Rats, Sprague-Dawley
  • Subarachnoid Hemorrhage / drug therapy*
  • Subarachnoid Hemorrhage / immunology
  • Subarachnoid Hemorrhage / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Xanthophylls / pharmacology

Substances

  • Interleukin-1beta
  • NF-kappa B
  • Neuroprotective Agents
  • Tumor Necrosis Factor-alpha
  • Xanthophylls
  • astaxanthine