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Objective: To study the protective effect of propofol precondition against glutamate (Glu) neurotoxicity to neonatal rat cerebrocortical slices., Methods: Brain slices of Sprague-Dawley (SD) rats were cultured in vitro and observed the morphologic changes. Brain slices were randomly divided into three groups: blank control group, Glu injury group (1 mmol/L Glu for 0.5 hour), propofol precondition group (20 mg/L propofol for 24 hours), each n=12. Changes in pathological and ultra-structure of cells were observed using microscope. Lactate dehydrogenase (LDH) leakage rate was measured. Meanwhile, the expression of glial fibrillary acidic protein (GFAP) was detected by immunohistochemical technology, then the positive cell were counted., Results: Cultured brain slices of cell were intact and survived well. Hematoxylin-eosin (HE) staining, electron microscopy and LDH test results showed that cerebral film neuron severely damage, gliosis, edema, LDH leakage rate in Glu injury group were significantly more severe compared with blank control group [(68.5±2.0)% vs. (16.0±2.5)%, P<0.01]. Reduce the brain slice of the propofol pretreatment group of neuronal cell jury, cell shape recovery significantly reduced LDH leakage rate compared with the Glu injury group [(38.5±2.4)% vs. (68.5±2.0)%, P<0.05]. Immunohistochemical detection of GFAP expression of Glu injury group glial cell body swelling, producing increase in the number of GFAP positive reaction strong, the number of positive cells compared with blank control group was significantly increased (50±5 cells/HP vs. 10±3 cells/HP, P<0.01). The recovery of propofol pretreatment group glial cell morphology, cell processes slender GFAP positive reaction decreased the number of positive cells compared with the Glu injury group was significantly decreased (30±4 cells/HP vs. 50±5 cells/HP, P<0.05)., Conclusion: Propofol pretreatment has protective effect against Glu injured rat cerebrocortical slices.

Objective: To investigate the protective effect of combined pretreatment of edaravone and propofol on cerebral cortex with ischemia/reperfusion (I/R) injury and its therapeutic window., Methods: Sprague Dawley (SD) rat brain cortex cells harvested within 24 hours of birth were cultured in vitro for 7 days. The cells were then divided into blank control group, glutamate injury group, 24-hour drug precondition control group, and 24-, 2-, 0-hour drug precondition groups according to random number table. The nerve cells in each pretreatment group were cultured in medium containing 100 μmol/L of edaravone and 3 mg/L of propofol 24, 2, or 0 hour before glutamate damage (200 μmol/L for 0.5 hour). Nerve cell survival or damage was determined by methyl thiazolyl tetrazolium (MTT), lactate dehydrogenase (LDH) leakage rate, and nerve cell Na+-K+-ATPase activity. The oxidation and anti-oxidation ability of nerve cells was observed by determining superoxide dismutase (SOD) activity (xanthine oxidase), malondialdehyde (MDA) content (thiobarbituric acid). Nerve apoptosis was detected by flow cytometry., Results: Compared with blank control group, in the glutamate injury group, nerve cell survival rate [(62.2±23.4)% vs. (90.5±14.8)%], the activity of SOD (U/ml: 6.864±2.872 vs. 29.569±3.684), Na+-K+-ATPase activity [U×mg(-1)×h(-1): 0.318±0.146 vs. 0.636±0.168] were significantly decreased, and rate of neuronal apoptosis [(9.4±0.7)% vs. (6.1±0.2)%], the content of MDA (nmol/ml: 0.515±0.101 vs. 0.294±0.105), LDH leakage rate [(41.2±1.6)% vs. (36.8±4.6)%] were significantly increased (P<0.05 or P<0.01). Compared with glutamate injury group, the cell survival rate and the activity of SOD and Na+-K+-ATPase were significantly increased in the drug pretreatment groups, and apoptosis rate, MDA content, and LDH leakage rate were significantly decreased with time-department, and effect in the 24-hour pretreatment group was most significant [survival rate of cell: (89.2±30.3)% vs. (62.2±23.4)%, SOD activity (U/ml): 17.780±4.514 vs. 6.864±2.872, Na+-K+-ATPase activity [U×mg(-1)×h(-1)]: 0.541±0.052 vs. 0.318±0.146, the rate of cell apoptosis: (6.7±0.4)% vs. (9.4±0.7)%, the content of MDA (nmol/ml): 0.319±0.101 vs. 0.515±0.101, LDH leakage rate: (37.2±1.4)% vs. (41.2±1.6)%, all P<0.01]., Conclusion: The synergistic protective effect of pretreatment with edaravone combined with propofol on neonatal rat brain cortex cells with I/R injury in vitro was evident; and 24-hour pretreatment is the best time window of protection for the cerebral neurons.