RESUMO
Objective@#To evaluate the role of 2B-containing NMDA receptors (NR2B) in sevoflurane anesthesia-induced cognitive dysfunction in aged rats.@*Methods@#Thirty-two healthy male Sprague-Dawley rats, aged 18 months, weighing 570-630 g, were divided into 4 groups (n=8 each) using a random number table method: control group (group C), sevoflurane anesthesia group (group S), sevoflurane anesthesia plus NR2B specific inhibitor Ro 25-6981 group (group S+ RO) and Ro 25-6981 group (group RO). S and S+ RO groups inhaled 3% sevoflurane for 4 h. Ro 25-6981 1 mg/kg was intraperitoneally injected at 15 min before inhaling sevoflurane in group S+ RO.Morris water maze test was performed at 2 days after the end of anesthesia to assess cognitive function.The rats were then sacrificed, and hippocampal tissues were obtained for determination of the expression and phosphorylation of ERK1/2 by Western blot.@*Results@#Compared with group C, the escape latency was significantly prolonged, the frequency of crossing the original platform was reduced, the time of staying at the original platform quadrant was shortened, and the phosphorylation of ERK1/2 was decreased in group S (P<0.05), and no significant change was found in the escape latency in S+ RO and RO groups (P>0.05). Compared with group S, the escape latency was significantly shortened, the frequency of crossing the original platform was increased, the time of staying at the original platform quadrant was prolonged, and the phosphorylation of ERK1/2 was increased in group S+ RO(P<0.05). There was no significant difference in ERK1/2 expression among the four groups (P>0.05).@*Conclusion@#The mechanism by which sevoflurane anesthesia induces cognitive dysfunction is related to up-regulating the expression of NR2B and inhibiting the activity of ERK1/2 in aged rats.
RESUMO
Objective To evaluate the role of 2B-containing NMDA receptors(NR2B)in sevoflu-rane anesthesia-induced cognitive dysfunction in aged rats.Methods Thirty-two healthy male Sprague-Dawley rats,aged 18 months,weighing 570-630 g,were divided into 4 groups(n＝8 each)using a ran-dom number table method: control group(group C),sevoflurane anesthesia group(group S),sevoflurane anesthesia plus NR2B specific inhibitor Ro 25-6981 group(group S+RO)and Ro 25-6981 group(group RO).S and S+RO groups inhaled 3％sevoflurane for 4 h.Ro 25-6981 1 mg/kg was intraperitoneally injec-ted at 15 min before inhaling sevoflurane in group S+RO.Morris water maze test was performed at 2 days af-ter the end of anesthesia to assess cognitive function.The rats were then sacrificed,and hippocampal tis-sues were obtained for determination of the expression and phosphorylation of ERK1/2 by Western blot.Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform was reduced,the time of staying at the original platform quadrant was shortened,and the phosphorylation of ERK1/2 was decreased in group S(P＜0.05),and no significant change was found in the escape latency in S+RO and RO groups(P>0.05).Compared with group S,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,the time of staying at the original platform quadrant was prolonged,and the phosphorylation of ERK1/2 was increased in group S+RO(P＜0.05).There was no significant difference in ERK1/2 expression among the four groups(P>0.05).Conclusion The mechanism by which sevoflurane anesthesia induces cognitive dysfunction is re-lated to up-regulating the expression of NR2B and inhibiting the activity of ERK1/2 in aged rats.
