Effect of 17β estradiol on propofol-induced long-term cognitive dysfunction in developing rats: the relationship with hippocampal Glu/GABA

Objective To evaluate the effect of 17β estradiol on propofol-induced long-term cognitive dysfunction in developing rats and the relationship with hippocampal glutamate (Glu)/γ-aminobutyric acid (GABA). Methods Sixty healthy male Sprague-Dawley rats, aged 7 days, weighing 11-18 g, were divided into 5 groups (n=12 each) using a random number table method: dimethyl sulfoxide (DMSO) group, fat emulsion group (group F), 17β estradiol group (group E), propofol group (group P) and propofol plus 17β estradiol group (group P+ E).17β estradiol 600 μg/kg was subcutaneously injected in group E, and the equal volume of DMSO was given instead in group DMSO.Propofol 75 mg/kg was intraperitoneally injected in group P, and the equal volume of fat emulsion was given instead in group F. 17β estradiol 600 μg/kg was subcutaneously injected and 30 min later propofol 75 mg/kg was intraperitoneally injected in group P+ E.Injection was performed once every 24 h for 7 consecutive days in each group.Morris water maze test was performed at 60 days of age.The rats were sacrificed after the end of Morris water maze test and hippocampi were removed for determination of Glu content (by ultraviolet colorimetry method) and GABA content (using enzyme-linked immunosorbent assay) in hippocampal tissues.Glu/GABA ratio was calculated. Results There was no significant difference in the escape latency, the number of crossing the original platform, percentage of time spent in target quadrant, Glu content or Glu/GABA ratio between group DMSO, group F and group E (P>0.05). There was no significant difference in GABA content among the five groups (P>0.05). Compared with group F, the escape latency was significantly prolonged, the number of crossing the original platform was reduced, and the percentage of time spent in target quadrant, Glu content and Glu/GABA ratio were decreased in group P (P<0.05). Compared with group P, the escape latency was significantly shortened, the number of crossing the original platform was increased, and the percentage of time spent in target quadrant, Glu content and Glu/GABA ratio were increased in group P+ E (P<0.05). Conclusion 17β estradiol can improve propofol-induced long-term cognitive dysfunction and the mechanism may be related to maintaining hippocampal Glu/GABA balance in developing rats. Key words: Propofol; Estradiol; Cognition disorders; Glutamic acid; gamma-Aminobutyric acid; Hippocampus