| 脊髓损伤后神经轴突导向分子Semaphorin 3A表达的研究 |
|
Hits: 2130
Download times: 583
Received:April 12, 2020
|
| 作者 | Author | 单位 | Unit | E-Mail |
| 王国毓 |
WANG Guo-yu |
西安交通大学第二医院骨二科, 陕西 西安 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
|
| 程志坚 |
CHENG Zhi-jian |
西安交通大学第二医院骨二科, 陕西 西安 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
|
| 贺西京 |
HE Xi-jing |
西安交通大学第二医院骨二科, 陕西 西安 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
xijing_h@vip.om.com |
| 杨宝辉 |
YANG Bao-hui |
西安交通大学第二医院骨二科, 陕西 西安 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
|
| 李浩鹏 |
LI Hao-peng |
西安交通大学第二医院骨二科, 陕西 西安 710004 |
The Second Department of Orthopaedics, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, Shaanxi, China |
|
|
| 期刊信息：《中国骨伤》2021年34卷，第4期，第368-372页 |
| DOI：10.12200/j.issn.1003-0034.2021.04.015 |
| 基金项目:陕西省2018年重点研发计划（编号：2018SF-124） |
|
目的： 研究后脊髓损伤大鼠Semaphorin 3A表达的变化，探索脊髓损伤后轴突再生受到抑制的可能机制。
方法： 40只雌性健康SD大鼠，8周龄，体质量（210.00±9.88） g，随机分为对照组（A组，20只）和模型组（B组，20只）。A组仅切开T10全椎板及T9、T11部分椎板，对脊髓未作其他处理；B组切开T10全椎板及T9、T11部分椎板采用脊髓横切法制作脊髓损伤的动物模型。两组分别在术后3、7、14、28、42 d （每组每个时间点4只）进行灌注、获取脊髓组织，然后进行HE染色，同时按照SP试剂盒的操作步骤进行Semaphorin 3A的表达。
结果： 单纯脊髓横切损伤后，损伤局部发生出血坏死，局部水肿，神经变性、坏死以及囊腔形成，胶质细胞增生胶质瘢痕形成。对照组Semaphorin 3A只在灰质区有低水平表达。模型组术后3 d脊髓损伤损伤区Semaphorin 3A无表达，14 d时脊髓损伤损伤区Semaphorin 3A的表达显著增加，处在较高的水平，28 d时Semaphorin 3A的表达呈中等水平，42 d时Semaphorin 3A阳性表达恢复到正常水平。
结论： 脊髓损伤后Semaphorin 3A表达升高，可能是抑制轴突再生的机制之一。 |
| [关键词]:脊髓损伤 组织病理 Semaphorin 3A |
| |
| Expression of Semaphorin 3A after spinal cord injury |
|
Abstract:
Objective: To investigate expression of Semaphorin 3A in rats after spinal cord injury and explore possible mechanism of inhibiting of axonal regeneration after SCI.
Methods: Forty healthy female SD rats,8 weeks old,weighing(210.00±9.88) g,were randomly divided into control group(20 rats in group A) and model group(20 rats in group B). In control group,removal of T10 lamina and partial removal of T9 and T11 lamina were performed,and no further operation was performed on spinal cord(pseudo-operation). In model group,the total T10 and partial T9,T11 partial lamina were incised and the spinal cord transection was performed to create animal models of spinal cord injury. The rats were perfused and spinal cord tissue obtained at 3,7,14,28 and 42 days after surgery(4 rats in each group at each time point),respectively,and then HE staining was performed. Meanwhile,the expression of Semaphoring 3A was detected in accordance with the protocol of SP kit.
Results: After a simple spinal cord transection injury,hemorrhagic necrosis,localized edema,neurodegeneration,necrosis,and cyst formation occurred in the injured area,and glial scar formation occurred in glial cells. Semaphorin 3A expression levels in control group was low in the gray matter area. There was no expression of Semaphorin 3A in the injured area of spinal cord injury in model group 3 days after operation. On the 14th day,the expression of Semaphorin 3A in the injured area of spinal cord injury increased significantly and was at a high level. On the 28th day,the expression of Semaphorin 3A was moderate. On the 42th day,the positive expression of Semaphorin 3A returned to normal level.
Conclusion: The increased expression of Semaphorin 3A after spinal cord injury may be one of the mechanisms that inhibit axonal regeneration. |
| KEYWORDS:Spinal cord injury Histopathology Semaphorin 3A |
| |
| 引用本文，请按以下格式著录参考文献： |
| 中文格式: | 王国毓,程志坚,贺西京,杨宝辉,李浩鹏.脊髓损伤后神经轴突导向分子Semaphorin 3A表达的研究[J].中国骨伤,2021,34(4):368~372 |
| 英文格式: | WANG Guo-yu,CHENG Zhi-jian,HE Xi-jing,YANG Bao-hui,LI Hao-peng.Expression of Semaphorin 3A after spinal cord injury[J].zhongguo gu shang / China J Orthop Trauma ,2021,34(4):368~372 |
|
| View Full Text View/Add Comment Download reader |
| Close |
|
|
|
