射频电磁场对人体健康影响日益受到重视，目前认为中枢神经系统海马是其敏感靶器官，如何进行有效防护是亟待解决的问题。我们前期实验证实蜕皮甾酮(EDS)对射频电磁场致海马功能障碍有显著防护作用。进一步研究发现，EDS可增加海马神经干/祖细胞内β-catenin表达。近期证实，肿瘤抑制基因PTEN调控的PI3K/Akt信号通路是影响神经干/祖细胞增殖的关键环节，而β-catenin正是其下游效应分子。据此，课题组提出"EDS通过影响海马神经干/祖细胞内PTEN调控的PI3K/Akt信号通路减轻射频电磁场致海马功能障碍"的假设，拟通过体内外实验，在PTEN的基因及蛋白水平进行干预，以期阐明：①射频电磁场暴露致大鼠海马PTEN表达变化规律及其与海马功能障碍的关系；②EDS如何通过PTEN调控的PI3K/Akt信号通路发挥保护效应？本课题将为射频电磁场致中枢神经系统功能障碍的机制与防护研究提供新的思路。

The dramatic increase in use of cellular telephones has prompted concerns regarding potential harmful effects of exposure to radiofrequency- modulated electromagnetic fields(RF-EMFs). Past studies have shown that hippocamp is sensitive to the exposure of RF-EMFs. However, there is no acceptable therapeutic methods about this exposure. PI3K/Akt signaling pathways have been implicated to increase the proliferation and differentiation of NSCs by activation of β-catenin, and phosphatase and tensin homolog on chromosome ten(PTEN) is considered to be the key signaling molecules invoved up-stream of PI3K/Akt. Furthermore, our recent study proved that ecdysterone(EDS) could increase the expression of β-catenin in hippocampal neuron stem cells(NSCs), and play a significant neuroprotective effect. Conbined with these evidence,we hypothesized that EDS could affect the PTEN controled PI3K/Akt signaling pathways, leading to the induction of β-catenin and other mediators, which were involved in the neuroprotection of expoure to RF-EMFs. Here, we used a set of experiments in vivo or in vitro to elucidate the relationship between the PTEN controled PI3K/Akt signaling pathways and hippocampal injury of exposure to RF-EMFs, the neuroprotective mechanism of EDS . Our work may confer a new therapeutic target of exposure to RF-EMFs.