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首页> 外文期刊>CNS neuroscience & therapeutics. >Heme Oxygenase‐1 Mediated Memorial and Revivable Protective Effect of Ischemic Preconditioning on Brain Injury
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Heme Oxygenase‐1 Mediated Memorial and Revivable Protective Effect of Ischemic Preconditioning on Brain Injury

机译：血红素加氧酶-1介导的缺血预处理对脑损伤的纪念性和可恢复性保护作用

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Summary Aims Ischemic preconditioning ( IPC ) has short‐term benefits for stroke patients. However, if IPC protective effect is memorial and the role of the intracellular protective protein heme oxygenase‐1 ( HO ‐1) is not known. Methods Ischemic preconditioning and the corresponding sham control were achieved by blocking the blood flow of the left internal carotid artery for 20 min and 2 second, respectively, in rats. Both IPC and sham‐operated animals were divided into three groups and treated with PBS , the HO ‐1 inducer hemin, and the HO ‐1 inhibitor Znpp. Three weeks after IPC , brain ischemia–reperfusion injury was achieved by left middle cerebral artery obstruction for 45 min followed by 24‐h reperfusion. Results 2,3,5‐triphenyltetrazolium chloride staining and neurological dysfunction scoring showed IPC significantly reduced brain infarct area and improved neurological function occurred 3 weeks after IPC . Hemin treatment promoted whereas Zn PP blocked the benefits of IPC . Immunohistochemical analysis and Western blotting showed that the expression of HO ‐1 was higher in the border zone than in the necrotic core zone. The memorial IPC protection is independent of adenosine receptor A1R and A2aR expressions. Conclusions We found for the first time that the protective effect of IPC can be remembered to protect brain injury occurred after acute response disappear. The results indicate that interventional treatment can achieve protective effect for future cerebral injury not only through interventional treatment itself but also through the memorial and revivable IPC , eliminating the concern that temporary ischemia caused by interventional treatment may leave harmful effect in the brain.
机译：总结目的缺血预处理（IPC）对中风患者具有短期益处。但是，如果IPC的保护作用是纪念性的，并且细胞内保护性蛋白血红素加氧酶-1（HO -1）的作用尚不清楚。方法通过分别阻断大鼠左颈内动脉的血流20分钟和2秒，实现缺血预处理和相应的假手术控制。将IPC和假手术动物分为三组，分别用PBS，HO-1诱导剂血红素和HO-1抑制剂Znpp处理。 IPC后三周，左脑中动脉阻塞45分钟，然后再进行24小时再灌注，造成了脑缺血再灌注损伤。结果2,3,5-三苯基四唑氯化物染色和神经功能障碍评分显示IPC显着减少了脑梗死面积并改善了IPC 3周后的神经功能。血红素的治疗促进了锌聚丙烯的益处。免疫组织化学分析和Western印迹显示，HO -1在边界区的表达高于坏死核心区。 IPC的保护性独立于腺苷受体A1R和A2aR的表达。结论我们首次发现IPC可以保护急性反应消失后发生的脑损伤。结果表明，介入治疗不仅可以通过介入治疗本身，而且可以通过纪念性和可再生的IPC达到对未来脑损伤的保护作用，从而消除了由介入治疗引起的暂时性缺血可能在大脑中留下有害作用的担忧。

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