Abstract:Objective To investigate the protective effect and mechanism of monosialotetrahexosylganglioside sodium (GM1) on traumatic brain injury (TBI) in rats.Methods A total of 30 SD rats were divided into control group,NS group and GM1 group according to the random number table (n=10,each).In the control group,the rats were only openind skell window without TBI model prepared,while in the other two groups,TBI model was made by hydraulic controlled injury device.In three groups,BrdU was injected intraperitoneally for 5 days continuously to mark the newborn nerve cells.The rats in the control group and NS group were injected with 1 ml/d sterile normal saline for 10 days,and the rats in GM1 group were injected with 5 mg·kg-1·d-1 GM1 for 14 days.At 11th day after opening skell window,the Morris water maze was carried out for 5 days.Then the rats were perfused and the brains were frozen.The apoptosis of cortical cells was detected by TUNEL kit,and the neoneurons in corter were detected by NeuN/BrdU double immunofluorescence.Results There were significant differences in escape latency and platform crossing times among the three groups (P<0.01).The escape latency increased in the order of control group,GM1 group and NS group,and the number of platform crossing decreased in the order of control group,GM1 group and NS group.The results of TUNEL showed that there were barely apoptotic cells in the cerebral cortex of the control group,a small number of apoptotic cells in the GM1 group,and more apoptotic cells in the NS group(P<0.05).The results of NeuN/BrdU double immunofluorescence showed that there were no NeuN+/BrdU+ neoneurons in cortex of the control group,less NeuN+/BrdU+ newborn neurons in cortex of the NS group,and more NeuN+/BrdU+ neoneurons in cortex of the GM1 group.Conclusion GM1 may protect the injured cortical cells from apoptosis,promote the development of endogenous neurons in the injured cortex,and improve the cognitive function (such as learning and memory) of TBI rats.