Departments of Pharmacology & Neuroscience, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Brain Res. 2013 Jun 13;1514:83-90. doi: 10.1016/j.brainres.2013.01.023. Epub 2013 Jan 20.
The neuroprotection research in the last 2 decades has witnessed a growing interest in the functions of estrogens as neuroprotectants against neurodegenerative diseases including stroke. The neuroprotective action of estrogens has been well demonstrated in both in vitro and in vivo models of ischemic stroke. However, the major conducted clinical trials so far have raised concern for the protective effect of estrogen replacement therapy in postmenopausal women. The discrepancy could be partly due to the mistranslation between the experimental stroke research and clinical trials. While predominant experimental studies tested the protective action of estrogens on ischemic stroke using acute treatment paradigm, the clinical trials have mainly focused on the effect of estrogen replacement therapy on the primary and secondary stroke prevention which has not been adequately addressed in the experimental stroke study. Although the major conducted clinical trials have indicated that estrogen replacement therapy has an adverse effect and raise concern for long term estrogen replacement therapy for stroke prevention, these are not appropriate for assessing the potential effects of acute estrogen treatment on stroke protection. The well established action of estrogen in the neurovascular unit and its potential interaction with recombinant tissue Plasminogen Activator (rtPA) makes it a candidate for the combined therapy with rtPA for the acute treatment of ischemic stroke. On the other hand, the "critical period" and newly emerged "biomarkers window" hypotheses have indicated that many clinical relevant factors have been underestimated in the experimental ischemic stroke research. The development and application of ischemic stroke models that replicate the clinical condition is essential for further evaluation of acute estrogen treatment on ischemic stroke which might provide critical information for future clinical trials. This article is part of a Special Issue entitled Hormone Therapy.
在过去的 20 年中,神经保护研究领域对雌激素作为神经保护剂对抗包括中风在内的神经退行性疾病的作用产生了越来越大的兴趣。雌激素的神经保护作用在体外和体内缺血性中风模型中得到了很好的证明。然而,到目前为止,进行的主要临床试验对雌激素替代疗法在绝经后妇女中的保护作用提出了担忧。这种差异可能部分归因于实验性中风研究与临床试验之间的翻译错误。虽然大多数实验研究使用急性治疗方案测试雌激素对缺血性中风的保护作用,但临床试验主要集中在雌激素替代疗法对原发性和继发性中风预防的效果上,而这在实验性中风研究中没有得到充分解决。尽管进行的主要临床试验表明雌激素替代疗法有不良影响,并对长期雌激素替代疗法预防中风提出了担忧,但这些并不适合评估急性雌激素治疗对中风保护的潜在影响。雌激素在神经血管单元中的作用已得到充分证实,其与重组组织纤溶酶原激活剂(rtPA)的潜在相互作用使其成为与 rtPA 联合治疗急性缺血性中风的候选药物。另一方面,“关键期”和新出现的“生物标志物窗口”假说表明,在实验性缺血性中风研究中,许多临床相关因素被低估了。开发和应用复制临床状况的缺血性中风模型对于进一步评估急性雌激素治疗缺血性中风至关重要,这可能为未来的临床试验提供关键信息。本文是专题题为“激素治疗”的一部分。