Many traditional Chinese medicines, including
Danhong injection (DHI), can be used to treat
cerebral ischemia-
reperfusion injury and have
neuroprotective effects on the brain; however, few studies have explored the mechanism by which this effect is generated. In this study, we investigated the
neuroprotective effect of DHI against
cerebral ischemia-
reperfusion injury mediated via the PI3K-Akt signaling pathway. After establishing the model of
middle cerebral artery occlusion (MCAO), 60 male Sprague-Dawley rats were allocated to six groups as follows:
sham, MCAO, DHI (MCAO + DHI),
LY294002 (MCAO +
LY294002 [PI3K-Akt pathway specific inhibitor]), DHI +
LY294002 (MCAO + DHI +
LY294002), and NMDP +
LY294002 (MCAO + NMDP [
nimodipine] +
LY294002).
Hematoxylin and
eosin (HE) and
terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining were used to evaluate the pathological changes of brain tissue and the degree of neuronal apoptosis. Real-time quantitative polymerase chain reaction (qRT-PCR), western blot analysis and
enzyme-linked
immunosorbent assays were used to measure the expression of Bad, Bax, Bcl-2, Bim, P53, MDM2, Akt, PI3K, p-Akt, p-PI3K, and Cyt-C. Compared with the MCAO group, brain tissue cell apoptosis was significantly reduced in the DHI group, and the brain function score was significantly improved. In addition, the expression of pro-apoptotic factors (Bad, Bax, and Bim) was significantly downregulated in the DHI group, while expression of the anti-apoptotic factor Bcl-2 was significantly upregulated, and expression of the apoptotic gene p53 was also significantly attenuated. Moreover, this
neuroprotective effect was attenuated by the PI3K-Akt signaling pathway inhibitor (
LY294002). Thus, our results confirmed the
neuroprotective effects of DHI in rats with
ischemia-reperfusion injury and indicate that these effects on the brain are partly generated by activation of the PI3K-Akt signaling pathway.