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[Research on motor dysfunction and the role of CTP after traumatic brain injury in rats].

OBJECTIVE
This is a study on the level of molecular biology to clarify the possible mechanism of delayed neural death after traumatic brain injury (TBI) and to probe into the influences of motor function of cytidine triphosphate(CTP) on rats after brain trauma.


METHOD
The model of severe closed traumatic brain injury (TBI) was established according to the method created by Marmarou in 1994. 300 Wistar rats were divided randomly into TBI group (n = 96), CTP treating group and sham operation group, and each of these three groups was divided into 8 subgroups, namely, 3, 6, 12, 24, 48, 72, 168 and 336 hours. At the same time, the rest 12 rats were taken as the normal group for comparison. The CTP treating group after injury were treated with injection of CTP (30 mg/(kg.d)) in peritoneum; the TBI group, the sham operation group and the normal group were treated with normal saline for comparison at the same time and all were killed at each time point. Another 48 rats were divided randomly into 4 groups, namely, brain injury group, CTP treating group, sham operation group and the normal group, and their motor dysfuction was evaluated using Neurological Severity Score (NSS). The methods such as immunohistochemistry, TUNEL and NSS were used to dynamically observe the pathological changes in cortex of rats, the expression of P53 protein and the motor function after TBI.


RESULTS
The increased expression of P53 protein and neural apoptosis showed up in cortex and motor dysfunction occurred after TBI.


CONCLUSION
The increased expression of P53 protein may bring about nerve cell apoptosis after TBI. Motor dysfunction is the inevitable outcome of nerve cell apoptosis in cortex. CTP can reduce P53 protein expression and nerve cell apoptosis, and it can improve motor function.