摘要
Abstract
Objective:To study the regulation of NMDA-NO pathway on postoperative cognitive dysfunction (POCD) in mice treated by a subanesthestic-dosage of ketamine.Methods:Thirty mice were randomly divided into three groups(n =10 per group):blank control group(group A),surgery group(group B),and surgery plus ketamine group(group C).The mice in group B and C were subjected to the separation of left carotid artery.Mice in group C were intraperitoneally injected with a subanesthetic dose of ketamine(0.1 mg) during the surgery.The water maze test was performed on the 1st,3rd,5th and 7th day after operation.The hippocampus were taken at 9 h post-operation.The protein expression of N-methyl-D-aspartic acid receptor (NMDAR) 2B in hippocampus were determined by immunohistochemistry.NMDAR1,NMDAR2A,and NMDAR2B protein levels were detected by western blotting.The contents of interleukins(IL-6) and tumor necrosis factor(TNF-α) in hippocampus and the relative activity of nitric oxide synthase(NOS) were measured.Results:After 1 and 3 days of operation,the latency to find the platform of the group B was significantly increased,while percent time in the target quadrant of water maze was decreased.There was no significant difference in the latency and percent time in the target quadrant between group A and C (P ＞ 0.05).NMDAR2B located on CA1 region of hippocampus.It was strongly expressed in group B,moderately expressed in group A,and weakly expressed in group C.The IRS score,the protein expressions of NMDAR1,NMDAR2A and NMDAR2B as well as the relative activity of NOS in group B were significantly higher than those in group A and C(P＜0.05),but no significant difference was noted between group A and C(P ＞0.05).Conclusion:A subanesthestic-dosage of ketamine could antagonize NMDA receptors,inhibit the activity of NOS and reduce the release of inflammatory factors,thereby reducing the incidence of POCD.关键词
亚麻醉剂量氯胺酮/术后认知功能障碍/N-甲基-D-天冬氨酸受体/炎症因子Key words
subanesthetic ketamine/postoperative cognitive dysfunction/N-methyl-D-aspartic acid receptor/inflammatory factor分类
医药卫生
