The aim of the present study was to uncover the mechanism underlying the neuroprotection of Hemin‑mediated
neuroglobin (Ngb) in an in vivo model of
brain injury. Sixty healthy male Sprague-Dawley rats were randomly divided into 5 groups (n=12, each group):
sham surgery,
ischemia,
Hemin,
LY294002 (LY) and
Hemin + LY. Focal
cerebral ischemia was established by unilateral
middle cerebral artery occlusion. Neurological function and
cerebral infarction volume were evaluated 24 h following surgery. Expression of Ngb and Akt
mRNA was detected by RT‑PCR, and the expression of Ngb
protein and activation of the PI3K/Akt pathway were determined by western blot analysis. No visible damage in the brain and no neurological impairment in the
sham surgery group were observed. When compared with the
ischemia group,
Hemin treatment induced the upregulation of Ngb and Akt
mRNA, Ngb
protein and phosphorylation of Akt (pAkt).
Hemin treatment also improved neurological functions and reduced
infarct volume. By contrast, LY treatment increased
infarct volume, deteriorated neurological functions and significantly reduced expression of pAkt; however, Ngb
mRNA and
protein expression was unchanged. When compared with
Hemin alone, a combination of
Hemin and LY treatment induced more severe brain damage and markedly decreased the expression of pAkt. The results of the present study demonstrated that the PI3K/Akt signaling pathway, which is associated with cell survival, mediates the
neuroprotective effects of Hemin‑induced Ngb following
cerebral ischemia.