Effects of Dexmedetomidine on the Expression of Cytochrome C Oxidase in Neonatal Mouse Primary Hippocampal Neurons Cultured in Propofol

Abstract

To observe the effects of propofol and dexmedetomidine on the expression of cytochrome c oxidase in primary hippocampal neurons isolated from neonatal mice. C57 neonatal mice were sacrificed within 24 h of birth and hippocampal tissue was collected. Primary hippocampal neurons were cultured in vitro and then randomly divided into a control group (0 μM propofol and 0 μM dexmedetomidine), propofol group (20 μM propofol and 0 μM dexmedetomidine) and propofol+dexmedetomidine group (20 μM propofol and 10 μM dexmedetomidine). The neurons were incubated for 1 h. Neuron morphology was observed under a light microscope. The expression of cytochrome c protein was detected semiquantitatively by Western blot and immunofluorescence staining. Compared with those in the control group, the primary hippocampal neurons in the propofol group were morphologically degenerated, with sparse axons and dendrites; the expression of cytochrome c protein was significantly higher in the propofol group (p<0.0001). The morphology of primary hippocampal neurons in the propofol+dexmedetomidine group was similar to that of primary hippocampal neurons in the control group, with plump and bright cell bodies and thickened neurites intertwined in a neuron network; additionally, cytochrome c protein expression was significantly lower in the hippocampal neurons in the propofol+dexmedetomidine group than in the hippocampal neurons in propofol group (p<0.0001). Dexmedetomidine reversed propofol induced injury and morphological abnormalities of primary hippocampal neurons. The mechanism may be related to the downregulation of cytochrome c protein expression.