依托咪酯对大鼠脑缺血再灌注损伤的保护作用及机制

Protective effects and mechanism of Etomidate on focal cerebral ischemia-reperfusion injury in rats

目的探讨依托咪酯对大鼠脑缺血再灌注损伤的神经保护作用及其机制。方法将120只♂SD大鼠随机均分为假手术组、模型组和依托咪酯高、低剂量组,ip给予各组大鼠相应药物后,采用线栓法制备大脑中动脉栓塞再灌注模型,评价依托咪酯对大鼠脑缺血再灌注的保护作用。参照Bederson评分标准评价大鼠的神经功能损伤,采用TTC染色法观察大鼠的脑梗死体积,采用免疫组化法分析大鼠海马CA1区NAIP、caspase-3及caspase-7蛋白的表达,采用HE染色法观察大鼠脑组织的病理变化。结果与模型组比较,依托咪酯组大鼠的神经功能损伤和脑梗死容积明显减轻,大鼠海马CA1区NAIP蛋白的表达明显增强,caspase-3蛋白的表达明显减少;依托咪酯高、低剂量组间比较无明显差异;各组大鼠海马CA1区caspase-7蛋白的表达无显著差异。结论依托咪酯对大鼠脑缺血再灌注造成的脑损伤具神经细胞保护作用,其机制可能与上调NAIP蛋白的表达、抑制caspase-3蛋白的活化有关。

OBJECTIVE To explore the protective effects and mechanism of Etomidate on focal cerebral ischemia - reperfusion injury in rats. METHODS 120 male SD rats were treated using 2 h line switch method to induce the middle cerebral artery occlusion （MCAO）/reperfusion model. The protective effects on brain were observed after intraperitoneal injection of different doses of Etomidate. Bederson test was used to evaluate defect of nerve functions, and TFC staining method was used to observe cerebral infarction volume. HE staining method was used to observe the pathological changes of brain tissues, and immunohistochemistry method was used to investigate the expression levels of NAIP, caspase - 3 and easpase - 7. RESULTS Compared with model group, Etomidate alleviated the nerve function injuries, but reduced the cerebral infarction volume. Etomidate also increased the expression of NAIP, obviously reduced the expression of caspase - 3, and had no effect on the expression of caspase - 7. CONCLUSION Etomidate has protective effect on cerebral ischemia - reperfusion injury in rats. It may be related to induction of the protein expression of NAIP and inhibition of the activation of caspase - 3.