Effects of Simvastatin on Neurone-Specific Enolase Expression in Rats with Traumatic Brain Injury / 天津医药

ABSTRACT

Objective To study the effect of simvastatin (SIM) on the expression of neuron specific enoalse (NSE) in rat brain and serum after traumatic brain injury (TBI), and therapeutic effects of SIM on TBI thereof. Methods A total of 90 Sprague-Dwalye (SD) rats aged 8 weeks were randomly divided into sham TBI group, control group and treatment group (n=30). The TBI model was established in control group and treatment group by using Feeney method. Rats in treatment group were fed SIM 10 mg/kg in the evening pre-injury and in every evening post-injury while those in control group were fed the same dose of starch at the same time. Blood samples (3 mL) were collected from carotid atrery in three groups, then rats were sacrificed and brains were collected at different time points (3 h, 12 h, 24 h, 3 d, 7 d and 14 d post-injury). The serum ex-pressions of NSE were detected by ELISA method. The NSE expressions in hippocampal area CA3 were detected with immu-nohistochemistry. Results (1) In control group, the serum NSE level was significantly increased at 3 h after injury, reached the peak at 3 d, and was still higher than that of sham injury group at 14 d. In treatment group, the serum NSE level was in-creased 3 h after injury, reached the peak at 24 h, decreased after 3 d, and was near the sham injury group at 14 d after inju-ry, but was significantly lower than that of control group. (2) Immunohistochemical detection showed that the NSE optical density values in hippocampal area CA3 area were decreased at 3 h after injury in control group. The optical density values reached the lowest level between 3 d to 7 d and were still significantly lower than those of sham injury group at 14 d. In treat-ment group the optical density value was decreased at 3 h after injury, reached the lowest level between 12 h to 24 h and re-bounded significantly at 7 d, then at 14 d up to the level of sham injury group. Conclusion SIM can promote the decrease of serum NSE level in TBI rats and increase the NSE expression of hippocampal neurons of injured side, showing protective effects on neuronal damage after traumatic brain injury.