Poinsatte Katherine, Selvaraj Uma Maheswari, Ortega Sterling B, Plautz Erik J, Kong Xiangmei, Gidday Jeffrey M, Stowe Ann M
Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center.
Department of Neurological Surgery, Washington University School of Medicine.
J Vis Exp. 2015 May 4(99):e52675. doi: 10.3791/52675.
Experimental animal models of stroke are invaluable tools for understanding stroke pathology and developing more effective treatment strategies. A 2 week protocol for repetitive hypoxic preconditioning (RHP) induces long-term protection against central nervous system (CNS) injury in a mouse model of focal ischemic stroke. RHP consists of 9 stochastic exposures to hypoxia that vary in both duration (2 or 4 hr) and intensity (8% and 11% O2). RHP reduces infarct volumes, blood-brain barrier (BBB) disruption, and the post-stroke inflammatory response for weeks following the last exposure to hypoxia, suggesting a long-term induction of an endogenous CNS-protective phenotype. The methodology for the dual quantification of infarct volume and BBB disruption is effective in assessing neurovascular protection in mice with RHP or other putative neuroprotectants. Adult male Swiss Webster mice were preconditioned by RHP or duration-equivalent exposures to 21% O2 (i.e. room air). A 60 min transient middle cerebral artery occlusion (tMCAo) was induced 2 weeks following the last hypoxic exposure. Both the occlusion and reperfusion were confirmed by transcranial laser Doppler flowmetry. Twenty-two hr after reperfusion, Evans Blue (EB) was intravenously administered through a tail vein injection. 2 hr later, animals were sacrificed by isoflurane overdose and brain sections were stained with 2,3,5- triphenyltetrazolium chloride (TTC). Infarcts volumes were then quantified. Next, EB was extracted from the tissue over 48 hr to determine BBB disruption after tMCAo. In summary, RHP is a simple protocol that can be replicated, with minimal cost, to induce long-term endogenous neurovascular protection from stroke injury in mice, with the translational potential for other CNS-based and systemic pro-inflammatory disease states.
中风的实验动物模型是理解中风病理和制定更有效治疗策略的宝贵工具。在局灶性缺血性中风小鼠模型中,为期2周的重复低氧预处理(RHP)方案可诱导对中枢神经系统(CNS)损伤的长期保护作用。RHP包括9次随机低氧暴露,其持续时间(2或4小时)和强度(8%和11%氧气)各不相同。在最后一次低氧暴露后的数周内,RHP可减少梗死体积、血脑屏障(BBB)破坏及中风后的炎症反应,提示内源性CNS保护表型的长期诱导。梗死体积和BBB破坏的双重定量方法可有效评估接受RHP或其他假定神经保护剂治疗的小鼠的神经血管保护作用。成年雄性瑞士韦伯斯特小鼠接受RHP预处理或与RHP持续时间相当的21%氧气暴露(即室内空气)。在最后一次低氧暴露2周后诱导60分钟的短暂大脑中动脉闭塞(tMCAo)。通过经颅激光多普勒血流仪确认闭塞和再灌注。再灌注22小时后,通过尾静脉注射静脉给予伊文思蓝(EB)。2小时后,通过异氟烷过量麻醉处死动物,脑切片用2,3,5-三苯基氯化四氮唑(TTC)染色。然后对梗死体积进行定量。接下来,在48小时内从组织中提取EB,以确定tMCAo后的BBB破坏情况。总之,RHP是一种简单的方案,可低成本重复实施,以诱导小鼠中风损伤的长期内源性神经血管保护,具有针对其他基于CNS和全身性促炎疾病状态的转化潜力。