Effects of Calpain Activity on Cognitive Function and Neuronal Apoptosis in Hippocampus of Rats after Traumatic Brain Injury

Objective:To approach the effects of calpain activity on hippocampal neuronal apoptosis and cognitive function in rats after traumatic brain injury (TBI).Methods:The rat model of severe closed traumatic brain injury was used.One hundred and twenty SD rats were divided randomly into TBI group,treated group,sham operation group and control group.The first 3 groups of 36 rats were further divided into five-phase groups,such as 6,12,24,48,72 h after injury (each subgroup n= 6).The calpain activity and neuronal apoptosis were observed in each subgroup.The cognitive function was tested in another 6 rats.There were 12 rats in control group.The calpain activity and neuronal apoptosis were observed in 6 rats of them and cognitive function was tested in another 6 rats.MDL28170 (10 μL) was injected into lateral ventricle of rats in treated group and isotonic Na chloride (10 μL) was injected in rats of TBI group,sham operation group and control group 1 d before TBI.Results:The calpain activity of the hippocampus was elevated in rats of TBI group at 6 h and peaked at 24 h.The calpain activity of the hippocampus was significantly lower at each time point in treated group than that of TBI group (P 0.01).A small amount of apoptosis-positive cells appeared in the CA2 area of hippocampus in TBI group at 6 h,significantly increased at 24 h and reached a peak at 72 h.The peak of apoptotic cell density was significantly reduced in treated group than that in TBI group (P 0.01).The results of place navigation proficiency test showed that the latency to search traffic island was significantly shorter in treated group than that of TBI group(P 0.01).The results of space exploration capability test results showed that the sailing time in the fourth quadrant was significantly longer in treated group than that in TBI group(P 0.01).Conclusion:The increased activity of calpain may result in neuronal apoptosis and cognitive dysfunction in rats after TBI.