Effects of propofol on amino acid neurotransmitter levels and neuronal apoptosis in the hippocampus in a rat model of ischemia/reperfusion injury

BACKGROUND: Excitatory amino acids including glutamic acid and aspartic acid play a neurotrophic role during early development of the central nervous system but go on to promote toxic effects. Inhibitory amino acids include gamma-aminobutyric acid and glycine. Changes in their concentration can reflect the degree of injury to brain tissue after cerebral infarction. OBJECTIVE: To investigate the effects of propofol on amino acid neurotransmitter levels and neuronal apoptosis in the hippocampus in a rat model of ischemia/reperfusion injury. DESIGN: Randomized controlled animal study. MATERIALS: Sixty male Wistar rats were randomly divided into a sham operation group, model group and propofol (50, 100 and 150 mg/kg) groups (n = 12). METHODS: Global brain models of ischemia/reperfusion injury were established in the model group and the propofol groups. The vertebral artery and common carotid artery were merely isolated in the sham operation group. Ten minutes before ischemia, rats in the propofol groups were induced with an intraperitoneal injection of propofol (50, 100 or 150 mg/kg); rats in the model and sham operation groups were induced with an intraperitoneal injection of saline (5 mL). MAIN OUTCOME MEASURES: Content of amino acids, neuronal apoptotic index and density of apoptotic neurons in the hippocampal CA1 region. RESULTS: After a 10-minute ischemia/60-minute reperfusion, the content of glutamic acid and aspartic acid was significantly decreased in the propofol (50, 100 and 150 mg/kg) groups compared with the model group (P < 0.05 or P < 0.01); but the content of gamma-aminobutyric acid was significantly increased in the propofol (100 and 150 mg/kg) groups (P < 0.05). After a 72-hour reperfusion, the neuronal apoptotic index was significantly decreased in the propofol (50, 100 and 150 mg/kg) groups compared with the model group (P < 0.05 or P < 0.01), and the decrease was remarkable in the propofol (100 and 150 mg/kg) groups. After a 72-hour reperfusion, neuronal apoptosis was not observed in the hippocampal CA I region in the sham operation group, and the density of apoptotic neurons in the propofol (50, 100 and 150 mg/kg) groups showed a significantly dose-dependent decrease in the hippocampal CA1 region compared with the model group (P < 0.01). CONCLUSION: Propofol can protect from brain ischemia/reperfusion injury. This is possibly related to inhibition of excitatory amino acid release, reduction in inhibitory amino acid consumption and decreasing neuronal apoptosis.