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Ischemic brain injury provokes complex, time-dependent downstream pathways that ultimately lead to cell death. We aimed to demonstrate the levels of a wide range of metabolites in brain lysates and their on-tissue distribution following neonatal stroke and cell therapies.
Metabolomic analysis of the injured hemisphere demonstrated that a variety of amino acids were significantly increased and that tricarboxylic acid cycle intermediates and some related amino acids, such as glutamate, were decreased. Although cell therapies did not ameliorate the changes in metabolites in the infarct area, mesenchymal stem cells ameliorated the increased levels of glutamate and carnitine in the peri-infarct area. These methodologies may be useful for further investigation of possible treatments for ischemic brain injury.
Neonatal encephalopathy is an important cause of mortality and cerebral palsy 1. Neonatal stroke is one of the most common causes of neonatal encephalopathy, and there has been no proven treatment for it 2. Recently, many researchers have focused on cell therapies because of their regenerative and neuroprotective effects.
The effects on injured neonatal brains are thought to be multifactorial, involving regeneration, paracrine effects and inflammatory modulation. Ischemic brain injury provokes complex, time-dependent downstream pathways that reach an inflammatory peak at approximately 24 h after injury.
