缺血预处理对大鼠创伤性脑损伤后脑组织细胞间黏附分子-1表达的影响

Effect of ischemic preconditioning on expression of intraceilular adhesion molecule-1 in brain tis- sues following traumatic brain injury in rats

目的探讨缺血预处理（ischemicprecoudition，IPC）对大鼠创伤性脑损伤（traumaticbraininjury，TBI）后脑组织细胞间黏附分子-1（intracellularadhesionmolecule-1，ICAM-1）表达的影响。方法雄性SD大鼠60只，体重220～250g，按随机数字表法分为假手术组、TBI组和IPC组，每组20只。短暂夹闭双侧颈总动脉制备脑IPC模型，采用Feeney自由落体撞击法制作TBI模型，假手术组仅行右侧顶部开窗而无TBI。分别于TBI后6，72h处死10只大鼠，取损伤脑组织，计算脑组织湿／干重比（W／D）值，采用免疫组化法测定ICAM-1表达水平，光镜观察病理学结果。结果与假手术组比较，TBI组脑组织W／D值升高（6h：4．2±0．4比2．7±0．4；72h：5．0±0．1比3．1±0．2，P〈0．05），脑组织ICAM-1表达上调（6h：25．4±3．5比8．6±1．3；72h：36．5±5．4比8．4±1．6，P〈0．05）；与TBI组比较，IPC组脑组织W／D值降低（6h：3．5±0．6比4．2±0．4；72h：3．7±0．4比5．0±0．1，P〈0．05），脑组织ICAM-1表达下调（6h：16．5±2．7比25．4±3．5；72h：24．3±4．6比36．54-5．4，P〈0．05）。IPC组脑组织损伤程度轻于TBI组。结论IPC可以下调脑组织ICAM-1表达，从而减轻大鼠TBI。

Objective To investigate the effect of ischemic preconditioning （IPC） on expression of intracellular adhesion moleeule-I （ICAM-1） in brain tissues following traumatic brain injury （TBI） in rats. Methods Sixty male SD rats weighing 220-250 g were randomly divided into three groups （ n = 20 for each） ： sham operation group, TB1 group, and IPC group. Cerebral IPC models were induced by transient occlusion of the bilateral common carotid arteries; TBI models were induced by Feeney＇ s free- falling method; rats in sham operation group were only performed exposure of dura of the right parietal lobe. Ten rats were sacrificed respectively at 6 and 72 hours after TBI and injured brain tissues were har- vested to estimate wet/dry weight （W/D） ratio for the brain, determine ICAM-1 expression by immuno- histochemistry and perform microscopic examination. Results Brain W/D ratio was significantiy in- creased in TBI group compared with sham operation group （6 h ： 4.2±0.4 vs 2.7± 0.4 ; 72 h ： 5.0 ± 0.1 vs 3.1 ± 0.2, P 〈 0.05 ）. ICAM-I expression was up-regulated in TBI group compared with sham operationgroup （6h： 25.4±3.5 vs8.6±1.3; 72 h： 36.5±5.4 vs 8.4±1.6, P〈0.05）. W/D ratio was significantly decreased in IPC group compared with TBI group （6 h ：3.5 ± 0.6 vs 4.2 ± 0.4 ; 72 h ： 3.7 ±0. 4 vs 5.0 ± 0.1, P 〈 0.05）. ICAM-1 expression was down-regulated in 1PC group compared with TBIgroup （6 h： 16.5 ±2.7vs25.4±3.5;72 h： 24.3 ＋4.6vs36.5±5.4, P〈0.05）. Milder injury to brain tissues was observed in ]PC group than in TBI group. Conclusion IPC can attenuate TBI in rats by down-regulating the expression of ICAM-I.