Propofol alleviates hypoxic neuronal injury by inhibiting high levels of mitochondrial fusion and fission.

ABSTRACT

OBJECTIVE: This study aimed to explore the mechanism of propofol in alleviating neuronal oxidative damage. MATERIALS AND METHODS: The neuron cells were randomly assigned to normal group (NOR), model group (MOD), and propofol administration group (MED). A 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was carried out to detect the viability of neuron cells, reverse transcription PCR (RT-PCR) assay to determine the gene expression of Fis and Mfn1, and Western blot assay to determine the protein expression of Caspase-3, Caspase-9, Bax, Bcl-2, and COX-2. RESULTS: According to the results of cell proliferation rate, under normal circumstances, neuron cells would have some programmed death and weak apoptosis, while after hypoxia-reoxygenation, the apoptosis rate of neuron cells gradually increased with the increase of culture time, which was significantly higher than that of the NOR. After the addition of propofol, the overall apoptosis rate of neuron cells slowly increased, significantly lower than that in the MOD and close to that in the NOR. Compared with the NOR, the ROS content in the MOD was significantly reduced, and compared with the MOD, the ROS content in the MED significantly recovered. Furthermore, the RT-PCR results showed that compared with the NOR, the expression of mitochondrial fusion protein (Mfnl) in the MOD group declined significantly, and the expression of mitochondrial fission protein 1 (Fis1) increased significantly, while after the addition of propofol, the expression of Mfnl and Fis1 was closed to that in the NOR. WB results showed that compared with the NOR, the expression of apoptosis proteins (Caspase-3, Caspase-9, Bax, and COX-2) in the MOD increased significantly, and the expression of Bcl-2 reduced significantly (all p<0.05), and the addition of propofol improved the expression of corresponding proteins. CONCLUSIONS: Propofol could alleviate hypoxic neuronal injury by inhibiting high levels of mitochondrial fusion and fission.