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.

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Sevoflurane is the most commonly used general anesthetic in pediatric patients. But preclinical studies indicate that sevoflurane could have neurotoxicity in newborn and old animals, and this raises concern regarding its safety. In this study, we explored the potential mechanisms of sevoflurane‐induced neurotoxicity in human SH‐SY5Y neuronal cells. We showed that prolonged exposure to 2% sevoflurane caused a significant increase in the Bag family protein Bag2 in a time‐ and dose‐dependent manner. We investigated the possible role of Bag2 upon exposure to sevoflurane by silencing Bag2 in neuronal cells. Knockdown of Bag2 caused increased overall reactive oxygen species (ROS) and generation of lipid peroxidation products 4‐hydroxynonenal (4‐HNE). Upon sevoflurane exposure, Bag2‐silent cells have reduced glutathione (GSH) and glutathione peroxidase activity. Under the sevoflurane treatment, Bag2‐deficient cells have reduced mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) production, while knockdown cells have less viability and higher lactic dehydrogenase (LDH) release as well as a higher percentage of apoptotic cells. The knockdown cells also had higher levels of mitochondrial cytochrome C release, a higher ratio of Bax/Bcl‐2 and increased caspase cleavage by sevoflurane. Overall, our data support an important role of Bag2 in sevoflurane‐induced neurotoxicity.