异氟烷预处理对脑缺血大鼠脑保护作用研究

目的：研究异氟烷预处理局灶性脑缺血成年大鼠模型,通过检测缺氧诱导因子1α( HIF-1α)、血红素氧合酶1(HO-1)以及 B 细胞淋巴瘤因子2(Bcl-2)表达水平揭示其脑保护作用。方法2月龄 SD 大鼠随机分为假手术组、单纯大脑中动脉闭塞模型组(MCAO 组)、异氟烷预处理组(ISO组),缺血再灌注采用90 min 大脑中动脉闭塞 MCAO,MCAO之前 ISO 组进行30 min 异氟烷预处理,30 min 空气洗脱。再灌注24 h 检测神经功能评分及脑梗死面积,MCAO 建模后再灌注6、24、72 h 收集大鼠脑皮层组织,Western blot 法检测HIF-1α、HO-1以及 Bcl-2表达水平。结果 MCAO 组术后24 h 改良神经损伤严重程度评分(mNSS 评分)明显低于 ISO组(P <0．05)。再灌注24 h 检测结果显示,ISO 组神经损伤及脑梗死面积明显小于 MCAO 组(P <0．05)。建模6、24 h后 MCAO 组和 ISO 组 HIF-1α、HO-1以及 Bcl-2表达水平显著上升(P <0．05),24 h 达到峰值,72 h 时间点各指标与假手术组间差异无统计学意义(P >0．05)。结论 ISO 预处理通过上调 HIF-1α、HO-1以及 Bcl-2表达发挥脑保护作用,但非长效作用。

Cerebral protective effect of isoflurance preconditioning for adult rat model with local cerebral ischemia

Objective To investigate the brain protective effects of isoflurane preconditioning for local cerebral is-chemia adult rat model by detecting HIF-1α, HO-1 and Bcl-2 expression level. Methods 84 two-month old Spra-gue-Dawley male rats were randomly divided into sham group, ischemia-reperfusion group ( MCAO group) and isoflurance preconditioning group (ISO group). ISO group was exposed to isoflurane for 30 min and then underwent a 90 min middle cerebral arterial occlusion (MCAO), while MCAO group underwent MCAO only. At 24 h after reperfusion all the groups were investigated by modified neurological severity score for neurological deficits, TTC staining for infarct percentage. Cerebral cortices were harvested for HIF-1α, HO-1 and Bcl-2 protein expression level detection at 6 h, 24 h and 72 h after reperfusion using RT-PCR and western blot. Results The mNSS score and infarct percentage in ISO group decreased significantly compared with those of MCAO group at 24 h after reper-fusion(P < 0. 05). Compared with the MCAO group, ISO group had significantly up-regulated protein levels of HIF-1α, HO-1 and Bcl-2 at 6 h and 24 h after reperfusion(P < 0. 05). There was no difference between ISO group and MCAO group for 3 gene expression at 72 h(P > 0. 05). Conclusion Isoflurane preconditioning plays short-term cerebral protective effect through the up regulation of HIF-1α, HO-1 and Bcl-2 gene expression.