Effects of dexmedetomidine post‑treatment on BDNF and VEGF expression following cerebral ischemia/reperfusion injury in rats.

Brain‑derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) serves a significant role in neural protection by activating the phosphatidylinositol 3‑kinase (PI3K)/Akt signaling pathway, which also was associated with the neuroprotective the treatment with dexmedetomidine (DEX). The present study aimed to further explore whether treatment with DEX post‑IR increased the expression level of BDNF and VEGF in the rat brain. A total of 30 healthy, clean male Wistar rats were randomly divided into 3 experimental groups: Control group, ischemia/reperfusion (I/R) group and DEX treatment group. Subsequently, BDNF and VEGF mRNA and protein expression levels were analyzed. The results indicated that the mRNA expression levels of BDNF and VEGF were higher in the I/R and DEX groups compared with expression levels in the Control group at 6 h and 1 day post‑treatment; the levels of BNDF mRNA expression were higher in the DEX group compared with the I/R group. The levels of BDNF and VEGF protein expression in the I/R and DEX groups were also significantly higher compared with those in the Control group. I/R surgery significantly increased the expression of BDNF and VEGF protein DEX group at 6 h, day 1 and day 3 compared with expression levels in the I/R group. Results from the present study indicated that post‑surgical treatment with DEX may increase the expression of BDNF and VEGF following I/R, which may serve a role in nerve protection.