Journal
NEUROBIOLOGY OF DISEASE
Volume 36, Issue 1, Pages 223-231Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2009.07.018
Keywords
Cerebral ischemia; Inflammation; Pyruvate; Stroke; Neuroprotection
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Funding
- Dept. of Veterans Affairs (MAY, RAS)
- NIH NINDS [R01 NS 40516]
- AHA [0540066N, P50 NS14543, P01 NS37520]
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Pyruvate, a key intermediate in glucose metabolism, was explored as a potential treatment in models of experimental stroke and inflammation. Pyruvate was administered to rodents after the onset of middle cerebral artery occlusion (MCAO). Since the extent of inflammation is often proportional to the size of the infarct, we also studied a group of animals given lipopolysaccharide (LPS) to cause brain inflammation without cell death. Following MCAO, pyruvate did not affect physiological parameters but significantly reduced infarct volume, improved behavioral tests and reduced numbers of neutrophils, microglial and NF kappa B activation. Animals given LPS showed increased microglial and NF kappa B activation which was almost completely abolished by pyruvate. Lactate, a major metabolite of pyruvate, was increased after pyruvate administration. However, administration of lactate itself did not have any anti-inflammatory effects. Pyruvate protects against ischemia possibly by blocking inflammation, but lactate itself does not appear to explain pyruvate's anti-inflammatory properties. Published by Elsevier Inc.
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