Department of Pharmacology, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China.
Department of Pharmacology, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China; Ningxia Key Laboratory of Craniocerebral Diseases of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, 750004, PR China.
Neurosci Lett. 2019 Oct 15;711:134415. doi: 10.1016/j.neulet.2019.134415. Epub 2019 Aug 10.
Hypoxic-ischemic brain damage (HIBD) leads to acute death and chronic neurological dysfunction in neonates. To date, there is no satisfactory acknowledged strategy to provide neuroprotection completely. Verbascoside (VB) has been proved to possess antioxidative, anti aging and neuroprotective activities. The aim of this study was to investigate whether VB provides neuroprotection to neonatal HIBD. Seven-day-old Sprague-Dawley rats were subjected to HIBD by permanent left carotid ligation for 2.5 h at 37 °C under hypoxic stress (8% O, 92% N). After VB treatment, early neurofunctions were assessed using the righting reflex and negative geotaxis reflex. 2, 3, 5-Triphenyltetrazolium chloride, Hematoxylin-Eosin, Nissl, and Fluoro-Jade B staining were used to evaluate the extent of brain damage. In addition, autophagy was observed by transmission electron microscopy, and the expression of autophagy-related proteins was measured using immunofluorescence and Western blot analysis. Results showed that administration of VB remarkably reduced neurofunctional latency, brain infarct volume, ameliorated neuronal damage and degeneration. Furthermore, VB decreased autophagosome formation, the Beclin-1 levels and LC3-II/I ratio with elevated levels of P62 in HIBD neonatal rats when compared to the HI group. These findings suggest that VB exerts potential neuroprotective effect against HIBD, which is at least partly to be mediated regulating autophagy.
缺氧缺血性脑损伤（HIBD）可导致新生儿急性死亡和慢性神经功能障碍。迄今为止，尚无完全令人满意的公认策略来提供神经保护。毛蕊花糖苷（VB）已被证明具有抗氧化、抗衰老和神经保护作用。本研究旨在探讨 VB 是否对新生儿 HIBD 提供神经保护。将 7 日龄 Sprague-Dawley 大鼠置于 37°C 下缺氧应激（8%O，92%N）2.5 小时，通过永久性结扎左侧颈总动脉建立 HIBD 模型。VB 治疗后，使用翻正反射和负向趋地反射评估早期神经功能。采用 2,3,5-三苯基四氮唑氯化物（TTC）、苏木精-伊红（HE）、尼氏和荧光金 B（Fluoro-Jade B）染色评估脑损伤程度。此外，通过透射电子显微镜观察自噬，通过免疫荧光和 Western blot 分析测量自噬相关蛋白的表达。结果表明，VB 可显著降低神经功能潜伏期、脑梗死体积，改善神经元损伤和变性。此外，与 HI 组相比，VB 降低了 HIBD 新生大鼠中自噬体形成、Beclin-1 水平和 LC3-II/I 比值，并增加了 P62 水平。这些发现表明 VB 对 HIBD 具有潜在的神经保护作用，这至少部分是通过调节自噬来介导的。
