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Neuroprotective effect of L‐serine against temporary cerebral ischemia in rats
Author(s) -
Wang GuoHua,
Jiang ZhengLin,
Chen ZhaoQin,
Li Xia,
Peng LiangLiang
Publication year - 2010
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22365
Subject(s) - neuroprotection , glutamate receptor , hippocampal formation , ischemia , pharmacology , nmda receptor , lactate dehydrogenase , serine , medicine , anesthesia , chemistry , biochemistry , endocrinology , receptor , enzyme
Abstract To investigate the neuroprotective effect of L‐serine and its underlying mechanisms, focal cerebral ischemia was induced in rats by occlusion of middle cerebral artery (MCAO) with a suture, and reperfusion was given by filament withdrawal 2 hr later. Meanwhile, rat hippocampal neurons were primarily cultured, and incubated in serum‐free medium in an incubator containing 1% O 2 for hypoxic exposure of 5 hr, or incubated in serum‐free medium containing 1 mM glutamate for glutamate exposure of 2 hr. Brain tissue injury and cell damage were then measured. L‐serine dose‐dependently decreased the neurology deficit score and infarct volume, elevated the cell viability and inhibited the leakage of lactate dehydrogenase. These effects were blocked by strychnine in both MCAO rats and cultured hippocampal neurons. Furthermore, L‐serine (168 mg·kg ‐1 ) reduced the brain water content, permeability of blood‐brain barrier, neuronal loss and the expression of activated caspase‐3 in the cortex. In addition, L‐serine effectively protected the brain from damage when it was administered within 6 hr after the end of MCAO. It is suggested that L‐serine could exert a neuroprotective effect on the ischemic‐reperfused brain and on the hypoxia‐ or glutamate‐exposed hippocampal neurons, which may be mediated by activating glycine receptors. © 2010 Wiley‐Liss, Inc.