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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 436429, 7 pages
Research Article

Metallothionein-II Inhibits Lipid Peroxidation and Improves Functional Recovery after Transient Brain Ischemia and Reperfusion in Rats

1Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suarez, Avenida Insurgentes Sur No. 3877, 14269 México City, DF, Mexico
2Laboratorio de Neuroprotección, Facultad de Farmacia, Universidad Autónoma del Estado de Morelos, Mexico
3Laboratorio de Neuropatología, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suarez, Mexico
4Departamento de Sistemas Biológicos de la Universidad Autónoma Metropolitana, Unidad Xochimilco México, Mexico

Received 14 November 2013; Revised 4 January 2014; Accepted 17 January 2014; Published 25 February 2014

Academic Editor: Verónica Pérez de la Cruz

Copyright © 2014 Araceli Diaz-Ruiz et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


After transient cerebral ischemia and reperfusion (I/R), damaging mechanisms, such as excitotoxicity and oxidative stress, lead to irreversible neurological deficits. The induction of metallothionein-II (MT-II) protein is an endogenous mechanism after I/R. Our aim was to evaluate the neuroprotective effect of MT-II after I/R in rats. Male Wistar rats were transiently occluded at the middle cerebral artery for 2 h, followed by reperfusion. Rats received either MT (10 μg per rat i.p.) or vehicle after ischemia. Lipid peroxidation (LP) was measured 22 h after reperfusion in frontal cortex and hippocampus; also, neurological deficit was evaluated after ischemia, using the Longa scoring scale. Infarction area was analyzed 72 hours after ischemia. Results showed increased LP in frontal cortex (30.7%) and hippocampus (26.4%), as compared to control group; this effect was fully reversed by MT treatment. Likewise, we also observed a diminished neurological deficit assessed by the Longa scale in those animals treated with MT compared to control group values. The MT-treated group showed a significant () reduction of 39.9% in the infarction area, only at the level of hippocampus, as compared to control group. Results suggest that MT-II may be a novel neuroprotective treatment to prevent ischemia injury.