Abstract
As a novel reactive oxygen species (ROS) scavenger, deuterohemin His peptide-6 (DhHP-6) has been demonstrated to prolong the lifespan of Caenorhabditis elegans and has also exhibited protective effects in myocardial ischemia-reperfusion injury. Whether similar effects occur during cerebral ischemia-reperfusion (CIR) injury remains to be elucidated. The present study evaluated the function of DhHP-6 and its underlying mechanisms in a middle cerebral artery occlusion (MCAO) model in rats. The focal transient MCAO model was implemented using the Longa method of ischemia for 2 h followed by reperfusion for 22 h in male Wistar rats. DhHP-6 was administered at the onset of reperfusion via intraperitoneal injection. The infarct volume, brain edema, brain apoptosis and neurological function were evaluated 24 h following stroke. To further determine the role of DhHP-6 in CIR injury, the levels of ROS and malondialdehyde (MDA), the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the protein expression levels of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), cleaved caspase-3, cytochrome c, Bcl-2 and phosphorylated-Akt/Akt were measured in ischemic cortex tissues. The results demonstrated that DhHP-6 significantly improved infarct volume, brain edema and neurological deficits, and reduced the percentage of TUNEL-positive cells. The levels of ROS and MDA were decreased, whereas no significant changes in the activities of SOD, CAT and GSH-Px were observed. The levels of Bax, cleaved caspase-3, and cytochrome c were downregulated, whereas the levels of Bcl-2 and p-Akt/Akt were upregulated. The results of the present study indicated that DhHP-6 may offer therapeutic potential for cerebral ischemia. The neuroprotective effects of DhHP-6 maybe mediated by its anti-oxidative properties, anti-apoptotic activities, or activation of the phosphoinositide 3-kinase/Akt survival pathway.
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