Abstract:Objecitve To investigate the neuroprotective effect of ginkgo lactone on traumatic brain injury (TBI) in rats and its possible mechanism. Methods A total of 36 SD rats (200-220 g) were purchased from Xuzhou Medical Animal Experimental Center.They were randomly divided into sham operated group, solvent group and ginkgo lactone group (n=12, each).The rats in the sham operation group were only craniotomy without TBI model.The rats in the solvent group and the ginkgo lactone group were molded TBI by hydraulic injury.All rats were intraperitoneally injected with BrdU after operation.The rats in the solvent group and the ginkgo lactone group were injected with solvent or ginkgo lactone through tail vein respectively.Blood samples were drawn from the tail vein at 1, 3, 7 and 14 days after operation to detect the levels of MDA and SOD.On the 15th day after operation, all rats underwent Morris water maze test for 5 consecutive days to observe the cognitive function of rats, then TUNEL method was used to detect the apoptosis of cells in the injured area, NeuN /BrdU double-labeling immunofluorescence was used to detect the neomature neurons in the cortex of the damaged area, and Western blot was used to detect the DCX protein in the hippocampus. Results The serum MDA levels in the solvent group and ginkgo lactone group increased at 1 d and 3 d, which were higher than those in the sham operation group(P<0.05); at 7 and 14 d, the solvent group was still higher than the sham operation group(P<0.05), while the ginkgo lactone group fell back to a level similar to the sham operation group(P>0.05). The serum SOD levels of the solvent group and ginkgo lactone group decreased at 1 d and 3 d, which were lower than that of the sham operation group(P<0.05); at 7 d and 14 d, the solvent group was still lower than the sham operation group(P<0.05), while the ginkgo lactone group recovered to a level similar to the sham operation group(P>0.05). The escape latency of rats in the cruise experiment decreased in the order of solvent group→ginkgo lactone group→sham operation group(P<0.01), and the platform crossing times of rats in the space exploration experiment decreased in the order of sham operation group→ginkgo lactone group→solvent group(P<0.01).No apoptotic cells were found in the cortex of rats in the sham operation group, more apoptotic cells were found in the cortex of rats in the solvent group, and the apoptotic cells in the cortex of rats in the ginkgo lactone group were significantly less than those in the solvent group (P<0.05).A small number of NeuN⁺/BrdU⁺double labeled mature neurons were found in the cortex of the solvent group, and more NeuN⁺/BrdU⁺double labeled mature neurons were found in the cortex of the injured area of the ginkgo lactone group (P<0.05).The expression level of DCX protein in hippocampus decreased in the order of sham operation group→ginkgo lactone group→solvent group (P<0.05). Conclusion Ginkgo lactone can reduce the level of oxidative stress in TBI rats, protect neurons from apoptosis, and promote the occurrence of neurons in the cortex and hippocampus of the injured area, so as to improve the cognitive function of TBI rats, such as learning and memory.