摘要
随着科学技术的不断发展，生物学家们逐渐意识到衰老也是一种可以治疗的疾病，因此人们开始关注延缓衰老的措施和方法。近10年来，促红细胞生成素（EPO）不仅具有以往我们所熟知的促进哺乳动物红系祖细胞增殖和分化的作用。EPO还可以通过抗氧化应激、抑制细胞凋亡等发挥神经保护作用。并且发现，EPO可以通过激活JAK2，从而激活P13K／Akt通路，使Nrf2从Nrf2：INrf2复合体上释放，转移至细胞核，与ARE反应元件结合促进抗氧化酶（如SOD、GSH等）的产生，达到抗氧化的作用。但是，在EPO参与的抗神经系统衰老的过程中是否通过激活P13K／Akt通路，调控Nrf2来发挥EPO的作用尚不清楚。为进一步探究EPO通过抗神经系统衰老的作用机制，本文回顾了EPO对神经系统保护作用的相关文章，进一步了解EPO抗氧化、抗凋亡等神经保护作用与P13K／Akt／Nrf2-ARE通路的关系。
With the development of science and technology the biologists gradually realize that aging is a disease which can be treated. Therefore the scientists concentrate on the measurements and methods of deferring aging. In the passed decades, it is found that EPO not only have the familiar effect of facilitating proliferation and differentiation on colony forming unit -erythroid （CFU -E） in mammal, but also have the effect of neuroprotection, such as the effect of anti - oxidation and anti - apoptosis in nervous system. In recent studies EPO can activate JAK2 and PI3K/Akt pathwway, then let Nrf2 dissociate from Nrf2：INrf2 complex in the cytosol. Finally Nrf2 is translocated to the nucleus, whereby it can bind to the ARE and promote the production of ROS （ such as SOD, GSH, and so on）. However whether EPO exerts its anti - aging effect in nervous system via PI3K/Akt pathway and induce Nrf2 is also unclear. This paper reviews plenty of articles on the neuroprotective effect of EPO and let us understand more information about the relationship between the anti - aging effect of EPO and PI3K/Akt/Nrf2 - ARE pathway are understood.
出处
《国际老年医学杂志》
2013年第6期265-269,共5页
International Journal of Geriatrics
基金
国家自然科学基金资助项目（81170330）,西安交通大学医学院第二附属医院重点项目[YJ（ZD）201003]
