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目的研究重组人促红细胞生成素(rhEPO)对急性脑缺血大鼠脑组织中核因子E2相关性因子2(Nrf2)及血红素加氧酶(HO-1)表达的影响,探讨rhEPO的抗氧化作用机制。方法随机将36只雄性SD大鼠分为假手术组、缺血组和rhEPO治疗组。采用线栓法制作大鼠永久性局灶性脑缺血(pMCAO)模型。rhEPO治疗组在缺血2h后腹腔注射rhEPO 5 000IU/kg,模型组和假手术组在等时间点给予等量的生理盐水。TTC(2,3,5-氯化三苯基四氮唑)法测量脑梗死体积,免疫组化方法测定脑组织中Nrf2及HO-1的表达。结果 rhEPO治疗组与缺血组相比,脑梗死体积减小,各组脑组织中Nrf2及HO-1的表达量按假手术组、缺血组、rhEPO治疗组依次增高,各组间差异均具有统计学意义(P<0.01)。结论急性脑缺血后,脑组织中Keap1-Nrf2/ARE抗氧化系统被激活,rhEPO可能通过激活该氧化系统而发挥脑保护作用。
Objective To investigate the effect of recombinant human erythropoietin (rhEPO) on the expression of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase (HO-1) in brain tissue of rats with acute cerebral ischemia Mechanism. Methods Thirty-six male SD rats were randomly divided into sham operation group, ischemia group and rhEPO treatment group. The rat model of permanent focal cerebral ischemia (pMCAO) was made by thread embolism. In the rhEPO group, intraperitoneal injection of rhEPO 5,000 IU / kg was performed 2 h after ischemia, and the model group and the sham operation group were given the same amount of normal saline at equal time points. The volume of cerebral infarction was measured by TTC (2,3,5-triphenyltetrazolium chloride) method, and the expression of Nrf2 and HO-1 in brain tissue were determined by immunohistochemistry. Results Compared with ischemic group, the volume of cerebral infarction was decreased in rhEPO-treated group. The expression of Nrf2 and HO-1 in each group were increased in sham-operated group, ischemic group and rhEPO-treated group With statistical significance (P <0.01). Conclusion After acute cerebral ischemia, the antioxidant system of Keap1-Nrf2 / ARE is activated in brain and rhEPO may play a neuroprotective role by activating this oxidative system.