Novel mechanisms for neuroprotective actions of erythropoietin

我们发现Epo在正常情况下增加了原代皮质培养细胞内Ca^<2+>浓度（[Ca^<2+>]I），但在兴奋毒性条件下降低了升高的[Ca^<2+>]I。epo诱导的增加涉及Ca^<2+>通过电压依赖性Ca通道内流，而epo诱导的减少涉及PI3激酶依赖的BK型Ca激活K通道的激活，至少部分。本研究结果的病理生理学意义有待进一步研究。

We found that Epo increased the intracellular Ca^<2+> concentration ([Ca^<2+>]I) in primary cortical cultures in the normal condition but decreased the elevated [Ca^<2+>]i in the excitotoxic condition. The Epo-induced increase involved Ca^<2+> influx through voltage-dependent Ca channels, whereas the Epo-induced decrease involved PI3 kinase-dependent activation of BK type Ca-activated K channels, at least in part. The pathophysiological significance of our findings needs to be investigated in further studies.