摘要
背景:脊髓损伤后胶质瘢痕和空洞的形成阻止了轴突进入远端,轴突再生能力极其有限,神经营养因子分泌不足,轴突生长的微环境中存在抑制因素等被认为是影响脊髓损伤患者功能恢复的主要因素。目的:分析国内外关于脊髓损伤后星形胶质细胞的生物学特性及胶质瘢痕增生的相关文献,以期为脊髓损伤后胶质瘢痕形成的相关机制研究提供理论依据。方法:以"astrocytes,reactive astrogliosis,glial scar,spinal cord injury"为关键词选择Pubmed数据库检索;以"星形胶质细胞,反应性星形胶质细胞增生,胶质瘢痕,脊髓损伤"为关键词选择万方数据库检索,对筛选出的62条文献进行分析。结果与结论:目前星形胶质细胞的生物学特性、反应性星形胶质细胞增生以及脊髓损伤后胶质瘢痕的研究已取得一定进展。研究主要致力于各种单一因子对脊髓损伤的影响,治疗也针对单一因素的干扰,而各因素之间的相互作用尚未完全明确;但在脊髓损伤后星形胶质细胞特定的细胞内、外信号分子的调节机制、脊髓损伤后胶质瘢痕形成的有效控制以及处理等方面仍需进一步深入研究。
BACKGROUND： Glial scar and cavity formation following spinal cord injury inhibits axonal entrance, so limited axonal regeneration, less secretion of neurotrophic factor and inhibitors in the microenvironment of axonal growth are considered as major impediments for impacting functional recovery of patients with spinal cord injury.OBJECTIVE： To analyze literatures home and abroad related to the biological characters of astrocytes and glial scar hyperplasia after spinal cord injury, and to provide a theoretical basis for the mechanism underlying glial scar formation following spinal cord injury. METHODS： Pub Med and Wanfang databases were retrieved using the keywords ＂astrocytes, reactive astrogliosis, glial scar, spinal cord injury＂ in English and Chinese, respectively. Finally 62 literatures were selected for overview. RESULTS AND CONCLUSION： Currently, studies concerning the biological characters of astrocytes, reactive astrogliosis and glial scar formation following spinal cord injury have achieved some progresses. Studies mainly focus on the sole impediment for spinal cord injury, and treatment also aims at inhibiting single factor, but interactions among factors have not been confimed. In addition, the regulatary mechanisms of specific intracellular and extracellular signal molecule in the astrocytes, and effective control and interference of glial scar formation following spinal cord injury still need in-depth study.
出处
《中国组织工程研究》
CAS
北大核心
2016年第37期5609-5616,共8页
Chinese Journal of Tissue Engineering Research
基金
国家自然科学基金支持项目(81560212)
内蒙古自然科学基金支持项目(2015MS0898)~~
