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促红细胞生成素（EPO）及其受体在人及动物脑中广泛存在,以自分泌或旁分泌方式发挥作用。脑缺氧缺血后脑中EPO mRNA表达增多,并具有内源性保护作用,外源性EPO可使其保护作用加强。目前认为脑缺氧缺血后EPO发挥保护作用的机制可能是增加细胞钙内流、保护神经元免受兴奋性氨基酸毒性作用、抑制一氧化氮过度合成及阻止神经元细胞凋亡等。
Erythropoietin (EPO) and its receptors are widespread in the human and animal brain and function in an autocrine or paracrine manner. The expression of EPO mRNA in brain increased after hypoxic-ischemic brain injury and had endogenous protective effect. Exogenous EPO could enhance its protective effect. Now that the mechanism of EPO protective effect after hypoxic-ischemic brain damage may be to increase cellular calcium influx, protect neurons from the excitotoxic amino acid toxicity, inhibit nitric oxide over-synthesis and prevent neuronal apoptosis.