延龄草根茎皂苷（TSTT）作为民间药物，对治疗跌打损伤、神经衰弱、癌症和炎症性疾病有显着疗效。然而，TSTT诱导缺血后神经血管恢复的机制尚未完全阐明。本研究旨在研究TSTT在促进缺血大鼠神经血管内源性修复、增强空间学习和记忆保留能力方面的价值。通过磁共振成像（MRI）实验观察TSTT对脑梗死和灌注的影响，并进一步探讨其分子机制。首先结扎大鼠大脑中动脉，构建永久性缺血模型，随后灌胃注射TSTT（120， 60, 30 mg kg-1) 术后 6 小时，然后在接下来的 30 天内每天一次。采用Morris水迷宫观察神经行为变化。进行多模态 MRI 序列来监测脑损伤和脑血流量。采用组织病理学染色来评估神经元的形态变化。采用透射电子显微镜（TEM）来检测神经元、血管结构和突触。利用免疫荧光染色来评估内源性修复进展。采用蛋白质印迹法分析轴突生长抑制剂和轴突引导线索。与模型组相比，TSTT减少了梗塞并增加了实质体积。值得注意的是，TSTT 治疗显着降低了 ADC（同侧/对侧）。在组织病理学检查中，TSTT显着增加了皮质和纹状体神经细胞的数量，并保护了神经血管单元的超微结构。根据核磁成像结果，TSTT增强了内源性修复进展。特别是，TSTT治疗明显抑制了NogoA/NgR/RhoA/ROCK2的蛋白水平，同时Netrin/DCC和Slit2/Robo1的表达增加。总而言之，我们的数据表明TSTT促进了大脑重建。上述结果与改善脑血流量、提高神经血管结构的完整性、加速内源性修复和损害轴突生长抑制剂NogoA/NgR/RhoA/ROCK2信号传导，从而改善中风后学习和记忆相一致。版权所有©2024。由Elsevier出版有限公司。

Trillium tschonoskii rhizome saponins (TSTT) has been significantly effective in treating traumatic injury, neurasthenia, cancer and inflammatory diseases as a folk medicine. However, the mechanism regarding to TSTT induced the neurovascular restorative after ischemia is without fully elucidated.This research was constructed to study the value of TSTT in promoting endogenous repair of neurovascular and augmenting the ability of spatial study and memory retention in ischaemic rats.The improvement of TSTT on cerebral infraction and perfusion was observed by magnetic resonance imaging (MRI) experiments and the molecular mechanisms were further explored.First, rats were ligated the middle cerebral artery to construct a permanent ischaemia model, subsequently intragastric injection administrated with TSTT (120, 60, 30 mg kg-1) at 6 h after operation, then once a day during next 30 days. Morris water maze was applied to observe the neurobehavioral changes. Multimodal MRI sequences were performed to monitoring brain injuries as well as cerebral blood flow. Histopathological staining was employed to evaluate the morphological changes of neurons. Transmission electron microscopy (TEM) was employed to detect the neurons, vascular structure, and synapse. Immunofluorescent staining was utilized to evaluate the endogenous repair progress. The axonal growth-inhibitors and axonal guidance cues were analyzed using western blotting.Contrast to the model group, TSTT declined the infarction and elevated the parenchymal volume. Notably, treated with TSTT significantly decreased the ADC (ipsilateral/contralateral). In histopathologic examination, TSTT prominently boosted amounts of cortical and striatal nerve cells and protected ultrastructure of neurovascular unit. According with results of nuclear magnetic imaging, TSTT enhanced endogenous repair progress. Especially, TSTT treatments obviously inhibited protein levels of NogoA/NgR/RhoA/ROCK2, accompanied by increased expression of Netrin/DCC and Slit2/Robo1.To sum up, our data illustrated that TSTT promoted cerebral reestablishment. The above result was in line with improving cerebral blood flow, elevated integrity of neurovascular structure, accelerating endogenous restoration and impairing the axonal growth inhibitors NogoA/NgR/RhoA/ROCK2 signaling, thereby improving poststroke learning and memory.Copyright © 2024. Published by Elsevier GmbH.