Wang Xiaoting, Huang Xiaoqin, Yang Mengqi, Pan Xueying, Duan Meiyi, Cai Hui, Jiang Guimiao, Wen Xianlong, Zou Donghua, Chen Li
Department of Neurology, Wuzhou Red Cross Hospital, Wuzhou, Guangxi Zhuang Autonomous Region, 543002, China.
Department of Neurology, the First Affiliated Hospital of Guangxi Medical University , Nanning, Guangxi Zhuang Autonomous Region, 530021, China.
Transl Neurosci. 2020 Nov 25;11(1):428-438. doi: 10.1515/tnsci-2020-0127. eCollection 2020.
The aim of this study was to investigate the neural plasticity in contralesional cortex and the effects of tongxinluo (TXL) in cerebral ischemic rats.
We used stroke-prone renovascular hypertensive (RHRSP) cerebral ischemia rat models to study the effect of TXL and the underlying mechanisms. We performed foot-fault and beam-walking tests to evaluate the motor function of rats after cortical infarction. Biotinylated dextran amine (BDA) was used to track axonal sprouting and neural connections.
TXL enhanced the recovery of motor function in cerebral infarction rats. TXL increased axonal sprouting in the peri-infarcted area but not in the corpus callosum, indicating in situ origination instead of crossing between cortical hemispheres through the corpus callosum. TXL promoted the sprouting of corticospinal axons into the denervated side of spinal gray matter. The synaptophysin (SYN)-positive intensity in the peri-infarcted area of TXL-treated group was greater than that in the vehicle group. We observed co-localization of SYN with BDA-positive fibers in the denervated spinal cord gray matter in the TXL group, suggesting that axonal remodeling and synaptic connections were promoted by TXL.
TXL may promote the recovery of neurological function by promoting the axonal remodeling and synapse formation of motor neuronal fibers after focal cortical infarction in hypertensive rats.
本研究旨在探讨脑缺血大鼠对侧皮质的神经可塑性以及通心络(TXL)的作用。
我们使用易卒中型肾血管性高血压(RHRSP)脑缺血大鼠模型来研究通心络的作用及其潜在机制。我们进行了足误和横梁行走测试,以评估皮质梗死后大鼠的运动功能。使用生物素化葡聚糖胺(BDA)追踪轴突发芽和神经连接。
通心络增强了脑梗死大鼠运动功能的恢复。通心络增加了梗死周围区域的轴突发芽,但胼胝体未出现,表明是原位发生,而非通过胼胝体在皮质半球之间交叉。通心络促进皮质脊髓轴突向脊髓灰质失神经侧发芽。通心络治疗组梗死周围区域的突触素(SYN)阳性强度大于载体组。我们在通心络组失神经的脊髓灰质中观察到SYN与BDA阳性纤维的共定位,表明通心络促进了轴突重塑和突触连接。
通心络可能通过促进高血压大鼠局灶性皮质梗死后运动神经元纤维的轴突重塑和突触形成来促进神经功能的恢复。