Marios Dimopoulos Clinical Nutritionist, Author, Fellow of the American Council of the Applied Clinical Nutrition

Τρίτη, 4 Φεβρουαρίου 2014

Omega-3 emulsion reduces stroke damage

Omega-3February 20, 2013. On February 20, 2013 in the journal PLOS One, Columbia University researchers report a benefit for omega-3 fatty acid-rich triglyceride lipid emulsions in an experimental model of ischemic stroke.
Richard J. Deckelbaum and his associates induced stroke in ten-day old mice and exposed them to a low oxygen environment for 15 minutes. Groups of animals were intraperitoneally injected with triglyceride emulsions containing the omega-3 fatty acids EPA, DHA or both omega-3 acids; omega-6-rich triglyceride emulsions or saline before and/or after brain injury was induced. Twenty-four hours subsequent to blood flow restoration, the animals’ brains were examined for damage.
Treatment with EPA and DHA prior to brain injury reduced total infarct volume by an average of 43 percent, and by 47 percent when the fatty acids were given afterward. A triglyceride emulsion enriched with DHA alone was found to reduce infarct volume by 51 percent when administered immediately after injury as well as when given two hours later. Examination of brain tissue from mice that received DHA revealed that the benefit was maintained after eight weeks.
"Since mice have a much faster metabolism than humans, longer windows of time for therapeutic effect after stroke are likely in humans," Dr Deckelbaum commented.
“A number of pathways are likely involved in omega-3 triglyceride neuroprotection,” the authors write. “For example, chronic administration of DHA resulted in increases of DHA levels in brain mitochondria.”
They add that DHA could help inhibit programmed cell death and improve the mitochondria’s ability to handle excessive intracellular calcium resulting from ischemia. "In most clinical trials in the past, the compounds tested affected only one pathway,” Dr Deckelbaum noted. “Omega-3 fatty acids, in contrast, are very bioactive molecules that target multiple mechanisms involved in brain death after stroke."

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