Humanin prevents brain mitochondrial dysfunction in a cardiac I/R injury model

Myocardial ischemia-reperfusion (I/R) injury causes interferences in systemic circulation and damages not only the heart but also several vital organs including the brain. Nevertheless, limited information is available regarding the effect of cardiac I/R injury on the brain including the blood brain barrier (BBB) breakdown, brain oxidative stress and mitochondrial function. Recently, a novel peptide called humanin has been shown to exert potent neuroprotective effects. However, the effect of humanin on the brain under cardiac I/R injury has not yet been investigated. Forty-two male Wistar rats were divided into two groups; an I/R group which were subjected to a 30-minute left anterior descending coronary artery occlusion, followed by 120-minute reperfusion (I/R group: n = 36), and a sham group (n = 6). The I/R group was divided into six subgroups. Each subgroup was intravenously given either vehicle or humanin analog (84 μg/kg/day) at three different time points: pre-ischemia, during-ischemia and at the onset of reperfusion. At the end of the experimental protocol, animals were sacrificed, and the brains were removed for determination of mitochondrial function, oxidative stress and western blot analyses. I/R injury condition caused BBB breakdown, increased brain oxidative stress and mitochondrial dysfunction. Only pre-ischemic humanin treatment attenuated brain mitochondrial dysfunction, but it did not prevent BBB breakdown nor brain oxidative stress. Humanin treatment during ischemia and at the reperfusion period provided no neuroprotection. These findings indicate that humanin exerted neuroprotection during cardiac I/R injury via improved brain mitochondrial function.

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