Akt regulates β-catenin in a rat model of focal cerebral ischemia-reperfusion injury.

The present study aimed to investigate the effects of the phosphoinositide 3‑kinase (PI3K)/Akt signaling pathway on the Wnt/β‑catenin signaling pathway in rats with focal cerebral ischemia‑reperfusion injury. A total of 96 rat focal cerebral ischemia‑reperfusion models, established according to a modified version of Longa's method, were randomly divided into four groups: Sham‑operated (S), cerebral ischemia‑reperfusion injury (I), cerebral ischemia‑reperfusion + basic fibroblast growth factor (bFGF) post‑processing and, finally, cerebral ischemia‑reperfusion + bFGF post‑processing + PI3K inhibitor LY294002 (LY). Each group consisted of 24 rats and each group was divided into four subgroups according to the indicated reperfusion times of 12, 24, 48 and 72 h. The morphological changes of the cortical tissue and the cellular apoptosis were determined using hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase dUTP nick end labeling method, respectively. The expression levels of phosphorylated (p‑)Akt, glycogen synthase kinase‑3β (GSK‑3β) mRNA and β‑catenin in the cortical tissue were detected at different time‑points. The number of apoptotic cells and the expression levels of p‑Akt, GSK‑3β mRNA and β‑catenin in the I and LY groups were significantly higher compared with those in the S group (P<0.05). In the bFGF group, the number of apoptotic cells and the mRNA expression levels of GSK‑3β were significantly decreased, whereas the expression levels of p‑Akt and β‑catenin were significantly increased compared with those in the I and LY groups (P<0.05). In cerebral ischemia‑reperfusion injury, the PI3K/Akt signaling pathway regulated β‑catenin, the main member of the Wnt signaling pathway, via GSK‑3β, providing information to assist in further investigation of the mechanism of β‑catenin in ischemia‑reperfusion injury.