Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan, PR China; Department of Neurology, Henry Ford Hospital, Detrot, MI, United States.
Department of Neurology, Henry Ford Hospital, Detrot, MI, United States; Department of Physics, Oakland University, Rochester, MI, United States.
Exp Neurol. 2018 Jun;304:82-89. doi: 10.1016/j.expneurol.2018.03.001. Epub 2018 Mar 5.
In addition to thrombolysis, tissue plasminogen activator (tPA) can evoke neurorestorative processes. We therefore investigated the therapeutic effect of subacute intranasal administration of tPA post stroke on neurological recovery and on corticospinal innervation in mice. A transgenic mouse line, in which the pyramidal neurons and corticospinal tract (CST) axons are specifically labeled by yellow fluorescent protein (YFP) was employed. Adult CST-YFP mice were subjected to right unilateral middle cerebral artery occlusion (MCAo), and were randomly divided into groups treated with saline or tPA intranasally in the subacute phase. Pseudorabies virus (PRV)-614-monomeric red fluorescent protein (RFP) was injected into the left forelimb. The cervical spinal cord and brain were processed for fluorescent microscopy to detect YFP and RFP labeling. Primary embryonic neurons were cultured with tPA at different concentrations. Neurite length and branch numbers were then measured. In vivo, subacute tPA treatment significantly enhanced functional recovery (p < 0.05), and increased CST density in the denervated gray matter, and in the numbers of PRV-labeled neurons in bilateral cortices. The behavioral performance was significantly correlated with axonal density in the denervated spinal cord. In vitro, both neurite length and branch numbers significantly increased with concentration of tPA (p < 0.05). Our results demonstrate that tPA dose-dependently increases neurite outgrowth and branching of cultured cortical neurons. Subacute intranasal administration of tPA may provide enhance neurological recovery after stroke by promoting CST axonal remodeling.
除了溶栓外,组织型纤溶酶原激活剂(tPA)还可以引发神经修复过程。因此,我们研究了亚急性鼻内给予 tPA 对中风后神经恢复和皮质脊髓束(CST)传入的治疗作用。我们使用了一种转基因小鼠品系,其中锥体神经元和 CST 轴突被黄色荧光蛋白(YFP)特异性标记。成年 CST-YFP 小鼠接受右侧大脑中动脉闭塞(MCAo),并随机分为接受盐水或 tPA 亚急性鼻内治疗的组。假狂犬病毒(PRV)-614-单体红色荧光蛋白(RFP)被注射到左前肢。对颈脊髓和脑进行荧光显微镜检测以检测 YFP 和 RFP 标记。用不同浓度的 tPA 培养原代胚胎神经元。然后测量神经突长度和分支数量。在体内,亚急性 tPA 治疗显著增强了功能恢复(p<0.05),并增加了去神经灰质中的 CST 密度,以及双侧皮质中 PRV 标记神经元的数量。行为表现与去神经脊髓中的轴突密度显著相关。在体外,随着 tPA 浓度的增加,神经突长度和分支数量均显著增加(p<0.05)。我们的结果表明,tPA 浓度依赖性地增加了培养的皮质神经元的神经突生长和分支。亚急性鼻内给予 tPA 可能通过促进 CST 轴突重塑来增强中风后的神经恢复。