南方医科大学学报

南方医科大学学报 ›› 2019, Vol. 39 ›› Issue (03): 292-.doi: 10.12122/j.issn.1673-4254.2019.03.06

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右美托咪定可减轻大鼠胫骨骨折手术所致的术后认知功能障碍

张津玮，张小宝，钱海涛，崔吉正，顾小萍   

  • 出版日期:2019-03-20 发布日期:2019-03-20

Dexmedetomidine alleviates cognitive dysfunction induced by tibial fracture in rats

  • Online:2019-03-20 Published:2019-03-20

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摘要： 目的研究右美托咪定对大鼠胫骨骨折手术所致术后认知功能障碍的影响。方法第1阶段：选择16只雄性SD大鼠，随机 分为对照组和胫骨骨折组，于胫骨骨折手术造模后1、3、5、7 d分别测定两组大鼠行为学指标及海马区CX3CL1蛋白及CX3CL1 mRNA的表达变化。第2阶段：选择24只雄性SD大鼠，随机分为对照组、胫骨骨折组和胫骨骨折+CX3CL1中和抗体组。分别 测定各组大鼠行为学指标及海马区CX3CL1蛋白的表达变化。第3阶段：选择24只雄性SD大鼠，随机分为对照组、胫骨骨折组 及胫骨骨折+Dex组。分别测定各组大鼠行为学指标及海马区CX3CL1蛋白和CX3CL1mRNA的表达变化。结果造模后1、3、 5、7 d，胫骨骨折组大鼠的新异臂探索时间明显低于对照组（P<0.05）；胫骨骨折组大鼠海马区CX3CL1蛋白和CX3CL1 mRNA 的表达明显低于对照组（P<0.05）；胫骨骨折+CX3CL1 中和抗体组大鼠新异臂探索时间明显低于胫骨骨折组；胫骨骨折+ CX3CL1中和抗体组大鼠海马区CX3CL1蛋白的表达明显低于胫骨骨折组；Dex组大鼠新异臂探索时间明显长于胫骨骨折组 （P<0.05）；Dex组大鼠海马区CX3CL1蛋白及CX3CL1 mRNA的表达明显高于胫骨骨折组（P<0.05）。结论Dex可以通过提高 CX3CL1的表达减轻大鼠胫骨骨折手术所致的术后认知功能障碍。

Abstract: Objective To study the effect of dexmedetomidine (Dex) on cognitive dysfunction induced by tibial fracture in rats. Methods Sixteen male SD rats were randomized into control group and tibial fracture group, and the behavior indicators were measured on days 1, 3, 5 and 7 after tibial fracture and the expressions of CX3L1 protein and mRNA in the hippocampus were detected. Another 24 male SD rats were randomly divided into control group, tibial fracture group, and tibia fracture with CX3CL1 antibody group, and the behavior indicators and hippocampal CX3L1 protein expression were evaluated after corresponding treatments. In another experiment, we randomized 24 male SD rats into control group, tibial fracture group and tibial fracture with Dex treatment, and tested their hippocampal CX3L1 protein and mRNA expressions as well as the behavior indicators after the treatments. Results Compared with the control rats, the rats with tibial fracture spent significantly less time in the novel arm on days 1, 3, 5 and 7 after the fracture (P<0.05) with obviously lowered expressions of CX3L1 protein and mRNA in the hippocampus (P<0.05). In the rats with tibial fracture, treatment with CX3CL1 antibody further decreased the time spent in the novel arm (P<0.05) and the expression level of CX3L1 protein in the hippocampus (P<0.05); In contrast, treatment with Dex significantly increased the time spent time in the novel arm (P<0.05) and enhanced the hippocampal expressions of CX3L1 protein and mRNA in rats with tibial fractures (P<0.05). Conclusion Dex can alleviate cognitive dysfunction induced by tibial fracture in rats by increasing the expression of CX3CL1 in the hippocampus.