Abstract
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 (P < 0.05) 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.
Highlights
Stroke is a disabling condition with devastating consequences for patients
Lipid peroxidation (LP) was measured 22 h after reperfusion in frontal cortex and hippocampus; neurological deficit was evaluated after ischemia, using the Longa scoring scale
After transient cerebral ischemia and reperfusion (I/R), damaging events initiate as result of the suppression of energy production caused by the interruption of oxygen and glucose supply to brain
Summary
Stroke is a disabling condition with devastating consequences for patients. Worldwide, it accounts for approximately 5.5 million deaths annually, with 44 million disability-adjusted life-years lost. The prevalence of stroke is expected to increase significantly around the world [1] This condition, in addition to the serious health complications, generates high costs; health care for stroke survivors has been estimated to be $18.8 billion dollars in 2008. Oxidative stress is an important mechanism involved in this process, as the antioxidant defenses are upregulated in order to cope with the reactive oxygen (ROS) and nitrogen species. All these free radicals damage the membrane’s fatty acids through a deleterious process known as lipid peroxidation (LP) [7]
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