西维来司钠对脑出血模型大鼠脑组织损伤的保护作用研究

目的：研究西维来司钠对脑出血模型大鼠脑组织的保护作用及其机制。方法：取40只大鼠随机均分为假手术组、模型组和西维来司钠高、中、低剂量（200、80、30mg／kg）组，除假手术组大鼠行假手术外其余各组大鼠行手术建立脑出血模型。假手术组和模型组大鼠建模前30min尾静脉注射O．9％氯化钠注射液，西维来司钠各剂量组大鼠同法尾静脉注射相应药物。各组大鼠建模术后24h检测血肿周围脑组织中中性粒细胞弹性蛋白酶（NE）、一氧化氮（N0）及髓过氧化物酶（MPO）的含量和血肿脑组织中核转录因子KB（NF-κB）的表达。结果：与假手术组比较，模型组大鼠血肿周围脑组织中NE、NO、MPO含量均明显增加（P〈0．01），血肿脑组织中NF—κB表达明显增强（P〈0．01）。与模型组比较，西维来司钠高、中剂量组大鼠血肿周围脑组织中NE、NO、MPO含量均明显减少（P〈0．05或P〈0．01），血肿脑组织中NF—r．B表达明显减弱（P〈0．05或P〈0．01），西维来司钠低剂量组大鼠上述指标差异无统计学意义（P〉0．05）。结论：西维来司钠对脑出血模型大鼠的脑组织有明显的保护作用，其机制可能与NE、NO、MPO含量减少及NF-κB表达减弱有关。

Study on Protective Effects of Sivelestat Sodium on Cerebral Tissue Damage in Cerebral Hemorrhage Model Rats

OBJECTIVE： To study protective effects of sivelestat sodium on cerebral tissue damage in cerebral hemorrhage mod- el rats and its mechanism. METHODS： 40 rats were randomly divided into sham operation group, model group and sivelestat sodi- um high-dose, medium-dose and low-dose （200, 80 and 30 mg/kg） groups. Cerebral hemorrhage model was induced by surgery in all groups except sham operation group. Sham operation and model group were given intravenous injection of 0.9% Sodium chlo- ride solution via tail vein 30 min before modeling. All sivelestat sodium groups were given intravenous injection of relevant medi- cine via tail vein at the same time. The contents of NE, NO, MPO in cerebral tissue around the hematoma and the expression of NF-nB in cerebral tissue were observed 24 h after modeling. RESULTS： Compared with sham operation group, the contents of NE, NO and MPO in cerebral tissue around the hematoma and the expression of NF-nB in cerebral tissue were increased obviously in model group （P〈0.01）. Compared with model group, the contents of NE, NO and MPO in cerebral tissue around the hemato- ma and the expression of NF-κB in cerebral tissue were decreased significantly in sivelestat sodium high-dose and medium-dose groups （P〈0.05 or P〈0.01） ; there was no statistical significance in above index of sivelestat low-dose group （P〉0.05）. CON- CLUSIONS： Sivelestat sodium has a noticeable protective effect on cerebral tissue of cerebral hemorrhage model rats. The mecha- nism is probably related to the decrease in the contents of NE, NO and MPO and the expression of NF-κB.