Department of Neurology, The First Hospital of Shanxi Medical University , Shanxi , China.
Int J Neurosci. 2014 May;124(5):362-8. doi: 10.3109/00207454.2013.848439. Epub 2013 Oct 31.
rhEPO has previously been shown to exert neuroprotective action in focal cerebral ischemia. However, its mechanism is not clear. We established the model of permanent focal cerebral ischemia. rhEPO was administered (5000 IU/kg i.p.) 2 h later after the successful ischemia model in rhEPO group and increased translation of Nrf2 and HO-1 and decreased the H2O2 concentration in the brain confirming activation of the Keap1-Nrf2/ARE pathway. The results show that rhEPO activate Keap1-Nrf2/ARE pathway after ischemia to protect the brain tissue.
rhEPO 先前已被证明在局灶性脑缺血中具有神经保护作用。但其机制尚不清楚。我们建立了永久性局灶性脑缺血模型。在 rhEPO 组成功建立缺血模型后 2 小时给予 rhEPO(5000 IU/kg,腹腔内注射),并增加 Nrf2 和 HO-1 的翻译,降低脑中 H2O2 浓度,证实 Keap1-Nrf2/ARE 通路被激活。结果表明,rhEPO 在缺血后激活 Keap1-Nrf2/ARE 通路以保护脑组织。