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. 2018 Apr 10;15(6):4629–4636. doi: 10.3892/etm.2018.6049

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Copyright: © Lu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — Overexpression of HO-1 via recombinant adenovirus transfection reversed behavioral impairments induced by secondary brain damage in transient cerebral ischemia-reperfusion injury. Transient cerebral ischemia-reperfusion damage reduced the neurological score at 24 h following middle cerebral artery occlusion. Overexpression of HO-1 significantly attenuated the neurological deficit score compared with transient cerebral ischemia injury groups (vehicle and Ad groups). Data are presented as the mean ± standard deviation (repeats, n=6). **P<0.01 vs. the sham group; ***P<0.001 vs. vehicle; ^###P<0.001 vs. the Ad group. Ad, empty adenovirus vector; HO-1, heme oxygenase-1; Ad-HO-1, recombinant HO-1 adenovirus.