丙泊酚对大鼠脑缺血再灌注后脑水肿及 EGFR 与 ERK1／2磷酸化的影响

摘要

目的：观察丙泊酚对大鼠脑缺血再灌注后脑水肿及表皮生长因子受体（EGFR）和细胞外信号调节蛋白激酶（ERK1／2）磷酸化的影响。方法将60只 SD 大鼠按随机数字表法分为6组：假手术组（Sham 组）、大脑中动脉栓塞（MCAO）2 h 模型组（I 组）、MCAO 2 h 再灌注24 h 模型组（I／R 组）、丙泊酚预处理假手术组（Pro 组）、丙泊酚预处理 MCAO 2 h 模型组（Pro＋I 组）及丙泊酚预处理 MCAO 2 h 再灌注24 h 模型组（Pro＋I／R 组），每组10只。将各组制模成功后大鼠断头取脑组织，采用干重法测定缺血区脑组织含水量，采用 Western Blot 检测 EGFR 和ERK1／2磷酸化水平。结果I／R 组缺血区脑组织含水量较 I 组和 Sham 组显著增加（P ＜0．05），EGFR 和 ERK1／2磷酸化水平较 I 组和 Sham 组显著升高（P ＜0．05）；Pro＋I／R 组脑组织含水量较 I／R 组显著降低（P ＜0．05），EG-FR 和 ERK1／2磷酸化水平较 I／R 组显著下降（P ＜0．05）。Sham 组、I 组、Pro 组、Pro＋I 组及 Pro＋I／R 组的缺血区脑组织含水量、EGFR 和 ERK1／2磷酸化水平比较差异均无统计学意义（P ＞0．05）。结论丙泊酚能有效通过抑制 EGFR 和 ERK1／2磷酸化降低脑缺血再灌注大鼠脑水肿程度。%ABSTRACT:Objective To observe the effects of propofol on brain edema and epidermal growth factor receptor(EGFR)and extracellular signal-regulated kinase 1/2(ERK1/2)phosphorylation in rats with cerebral ischemia/reperfusion injury.Methods Sixty SD rats were randomly divided into six groups:sham operation(sham group),middle cerebral artery occlusion(MCAO)for 2 hours(I group),MCAO for 2 hours + reperfusion for 24 hours(I/R group),sham operation+propofol preconditioning (Pro group),propofol preconditioning + MCAO for 2 hours (Pro + I group),and propofol preconditioning+MCAO for 2 hours+reperfusion for 24 hours(Pro+I/R group),with 10 rats in each group.After the model was successfully established,rats were decapi-tated and brain tissues were collected.Ischemic brain tissue water content was measured using dry-weight method.EGFR and ERK1/2 phosphorylation levels were determined by Western blot. Results Compared with I group or sham group,brain tissue water content and EGFR and ERK1/2 phosphorylation levels increased in I/R group(P <0.05).Compared with I/R group,brain tis-sue water content and EGFR and ERK1/2 phosphorylation levels decreased in Pro+I/R group (P <0.05).There were no significant differences in ischemic brain tissue water content and EG-FR and ERK1/2 phosphorylation levels among sham group,I group,Pro group,Pro+I group and Pro+I/R group.Conclusion Propofol can effectively reduce brain edema in rats with cerebral is-chemia/reperfusion injury through inhibiting EGFR/ERK1/2 phosphorylation.