ABSTRACT
Objective:To evaluate the effect of propofol on dopaminergic neurons of mice with Parkinson′s disease (PD).Methods:Forty-eight pathogen-free healthy male C57BL/6 mice, aged 8-12 weeks, weighing 22-32 g, were divided into 3 groups ( n=16 each) using a random number table method: control group (group C), group PD and propofol group (group Pro). The neurotoxin 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropypridine (MPTP) was intraperitoneally injected for 7 consecutive days in PD and Pro groups, while the equal volume of normal saline was given for 7 consecutive days in group C. At 30 min after intraperitoneal injection of MPTP, propofol 25 mg/kg was intraperitoneally injected in group Pro, while the equal volume of normal saline was given daily in group C and group PD.At day 8 after the end of establishment of the model, gait analysis system experiment and rotarod test were used to record the step distance and retention time.The animals were sacrificed after the behavioral tests, and the brain tissues were removed for the dopamine neuron count in substantia nigra (by immunohistochemistry) and for determination of the expression of alpha-Synuclein (α-Syn) and Tyrosine hydroxylase (TH) in the substantia nigra (by Western blot). Results:Compared with group C, the step distance was significantly decreased, retention time were shortened, the dopamine neuron count in substantia nigra was decreased, the expression of TH was down-regulated, and expression of α-Syn in substantia nigra was up-regulated in group PD ( P<0.05), and no significant change was found in the parameters mentioned above in group Pro ( P>0.05). Compared with group PD, the step distance was significantly increased, retention time were prolonged, the dopamine neuron count in substantia nigra was increased, the expression of TH was up-regulated, and expression of α-Syn in substantia nigra was down-regulated in group Pro ( P<0.05). Conclusion:Propofol has protective effect on dopaminergic neurons of PD mice, and the mechanism may be related to the down-regulation of α-Syn expression in substantia nigra.