期刊
NEURAL REGENERATION RESEARCH
卷 12, 期 3, 页码 478-485出版社
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.202921
关键词
nerve regeneration; spinal cord injury; epothilone B; pericytes; gene expression; fibrous scar; beta-tubulin; platelet-derived growth factor receptor beta; neuron-glial antigen 2; fibronectin; glial fibrillary acidic protein; rats; neural regeneration
资金
- Science and Technology Developing Program of Shandong Provincial Government of China [2010GSF10254]
- Medical and Health Science and Technology Plan Project of Shandong Province of China [2015WS0504]
Scar formation after spinal cord injury is regarded as an obstacle to axonal regeneration and functional recovery. Epothilone B provides moderate microtubule stabilization and is mainly used for anti-tumor therapy. It also reduces scar tissue formation and promotes axonal regeneration after spinal cord injury. The aim of the present study was to investigate the effect and mechanism of the microtubule-stabilizing reagent epothilone B in decreasing fibrotic scarring through its action on pericytes after spinal cord injury. A rat model of spinal cord injury was established via dorsal complete transection at the T10 vertebra. The rats received an intraperitoneal injection of epothilone B (0.75 mg/kg) at 1 and 15 days post-injury in the epothilone B group or normal saline in the vehicle group. Neuron-glial antigen 2, platelet-derived growth factor receptor , and fibronectin protein expression were dramatically lower in the epothilone B group than in the vehicle group, but -tubulin protein expression was greater. Glial fibrillary acidic protein at the injury site was not affected by epothilone B treatment. The Basso, Beattie, and Bresnahan locomotor scores were significantly higher in the epothilone B group than in the vehicle group. The results of this study demonstrated that epothilone B reduced the number of pericytes, inhibited extracellular matrix formation, and suppressed scar formation after spinal cord injury.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据