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

الملخص EN

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.