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Dexmedetomidine mitigates sevoflurane-induced cell cycle arrest in hippocampus

Li-Jun Bo, Pei-Xia Yu, Fu-Zhen Zhang, Zhen-Ming Dong

Background: Epidemiologic studies suggest the possibility of a modestly elevated risk of adverse neurodevelopmental outcomes in children exposed to anesthesia during early childhood. Sevoflurane is widely used in paediatric anaesthetic practice. It is urgent to search for neuroprotective strategies.

Materials and Methods: In our study, the hippocampal neuron cells were isolated from new-born neonatal rats and cultured in vitro. We performed immunocytochemistry with anti-MAP-2 and anti- GFAP antibodies to examine the purity of neurons. Cell cycle distribution was examined by flow cytometry. The protein levels of BDNF and TrkB were analysed via Western blot.

Results: Immunocytochemistry results showed that the purity of neurons>94%, which provided a good model for neural pharmacology experiments. The exposure of sevoflurane induced cell cycle arrest at S phase and suppressed the expression of BDNF and TrkB, and the exposure duration influenced the role of sevoflurane. In our study, the addition of DEX partly relieved the cell cycle arrest and the inhibitory of BDNF and TrkB expression induced by sevoflurane. What’s more, the function of DEX was in dosage-dependent manner and suppressed by a α2 adrenergic receptor blocker yohimbine.

Conclusion: Taken together, sevoflurane suppressed neurons cell proliferation via regulating the expression of BDNF and TrkB, and DEX relieved the neurotoxicity induced by sevoflurane via α2 adrenergic receptor.