Protective Effects of Dexmedetomidine on Hippocampal Neurons in Rats Anesthetized with Sevoflurane

Abstract

To explore effects of dexmedetomidine (Dex) on cognitive function and hippocampal neuronal apoptosis in rats anesthetized with sevoflurane (Sevo), and regulation of brain-derived neurotrophic factor (BDNF) and its downstream signaling. 30 Sprague-Dawley (SD) rats were randomly divided into control group inhaled 29% concentration oxygen), Sevo group (2 L/min oxygen flow +1.5% Sevo), Dex+Sevo group (after injection of 20 μg/kg Dex, treated with 2L/min oxygen flow+1.5% Sevo). Haematoxylin and eosin (HE) staining and Nissl’s staining were adopted to detect morphological and functional changes in hippocampus of rats. Apoptosis was detected by immunofluorescence, BDNF expression was detected by immunohistochemistry. Reverse transcription PCR (RT-PCR) was conducted to detect mRNA expression of key proteins in downstream signaling of BDNF. The results showed that Sevo induced apoptosis of hippocampus neurons, while Dex improved Sevo induced apoptosis. In contrast to the control, the positive expression of BDNF in hippocampus of Sevo group was notably decreased (P < 0.05), and that of Dex+Sevo group was notably higher in contrast to Sevo group (P < 0.05). Signaling pathways of MAPK, PI3K-Akt, and Ras were predicted by String software as the downstream pathways of BDNF. RT-PCR results showed that these 3 signaling pathways were involved in Dex improving Sevo-induced cognitive impairment and hippocampal neuron apoptosis. In conclusion, Dex could improve cognitive dysfunction and hippocampal neuron apoptosis in rats induced by Sevo, and the mechanism was related to upregulation of BDNF expression and activation of pathways of MAPK, PI3K-Akt, and Ras.