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Background: The use of anesthetics propofol in certain pediatric age groups remains off-label, but it may cause neuronal apoptosis, long-term cognitive and neurological abnormalities during early postnatal period. Dexmedetomidine (Dex) can exert neuroprotective effects in rats. This study aimed to evaluate the effects of Dex and propofol on the apoptosis of neonatal rat hippocampal neurons. Methods: Primary hippocampal neurons of neonatal rats were isolated and identified by immunofluorescence. Neurons were then divided into normal control, propofol (12 μg/ml propofol), and propofol+Dex group (12 μg/ml propofol+0.25 μg/ml Dex). The cell morphology was detected by Hematoxylin-Eosin (HE) staining. The cell apoptosis was analysed by flow cytometry and Hoechst assay. The expression of Bcl-2 mRNA and protein was determined by quantitative reverse transcription PCR and Western blot. Results: The apoptosis rate and proportion of Hoechst-positive cells in propofol group was significantly higher compared with control group (p=0.023 and 0.036, respectively). Propofol+Dex group exhibited significantly lower apoptosis and Hoechst-positive rate compared with propofol group (p=0.016 and 0.028, respectively). The expression of Bcl-2 mRNA and protein in propofol group was significantly decreased compared with control group (p=0.012 and 0.043, respectively). The Bcl-2 mRNA and protein expression in propofol+Dex group was significantly higher than those in propofol group (p=0.033 and 0.026, respectively). Conclusion: Propofol inhibited the growth and induced apoptosis of neonatal rat hippocampal neurons, whereas Dex suppressed the propofol-induced apoptosis via increasing the expression of Bcl-2. Our findings indicate that Dex in conjunction with propofol might reduce the propofol-induced neurotoxicity in pediatric patients who undergo general anesthetics, and therefore might provide an effective clinical measure against neural damages associated with general anesthetics.

Dexmedetomidine reduces propofol-induced apoptosis of neonatal rat hippocampal neurons via up-regulating Bcl-2 expression