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 ( < 0.05) with obviously lowered expressions of CX3L1 protein and mRNA in the hippocampus ( < 0.05). In the rats with tibial fracture, treatment with CX3CL1 antibody further decreased the time spent in the novel arm ( < 0.05) and the expression level of CX3L1 protein in the hippocampus ( < 0.05); In contrast, treatment with Dex significantly increased the time spent time in the novel arm ( < 0.05) and enhanced the hippocampal expressions of CX3L1 protein and mRNA in rats with tibial fractures ( < 0.05).@*CONCLUSIONS@#Dex can alleviate cognitive dysfunction induced by tibial fracture in rats by increasing the expression of CX3CL1 in the hippocampus.