基于BDNF-TrkB/proBDNF-p75NTR信号通路探讨电针治疗脊髓损伤的分子机制附视频

被引：0
|
作者：
叶青
时素华
姚海江
胡煜
曹祖懋
李志刚
机构：
[1] 北京中医药大学
来源：
河南中医 | 2023年 / 07期
关键词：
脊髓损伤; 电针疗法; 脑源性神经营养因子; 原肌球蛋白受体激酶B; 脑源性神经营养因子前体; p75神经营养素受体;
D O I：
10.16367/j.issn.1003-5028.2023.07.0219
中图分类号：
R245.97 [];
学科分类号：
摘要：
电针治疗脊髓损伤可以显著提高脑源性神经营养因子（brain-derived neurotrophic factor, BDNF）、原肌球蛋白受体激酶B（tropomyosin-receptor kinase, TrkB）蛋白的表达，下调p75神经营养素受体(p75 neurotrophin receptor, p75NTR)蛋白的表达。电针可以通过提高BDNF促进神经元的存活、促进受损纤维的再生、促进神经可塑性、促进髓鞘形成BDNF基因修饰的成纤维细胞。BDNF诱导的TrkB信号可能通过四种主要的细胞内途径影响突触可塑性、轴突生长、存活和细胞内阳离子平衡：（1）经磷脂酰-3激酶（P1-3K）/Akt通路促进神经元树突分枝和树突棘生成，影响突触生长和结构形成。（2）受体诱导小分子GTP酶Ras的激活，经过一系列复杂的磷酸化过程，最终激活许多细胞外信号调节激酶（extracellular signal-regulated Kinase, ERK）途径并对环腺苷3′,5′-单磷酸含量进行调节促进轴突生长。（3）经磷脂酶C-γ（Phospholipase C-γ,PLC-γ）/肌醇3-磷酸（inositol triphosphate, IP-3）通路参与Ca2+的调控，促进Ca2+从细胞内储存释放，促进突触可塑性等。（4）此外通过N-甲基-D-天冬氨酸（N-Methyl-D-aspartic acid, NMDA）受体的磷酸化，TrkB信号可能导致钙和钠内流的增加。故电针治疗脊髓损伤，可使BDNF与TrkB高亲和力结合，促进脊髓损伤的修复。其可能是通过激活BDNF-TrkB信号通路，抑制BDNF前体（brain-derived neurotrophic factor precursor, proBDNF）-p75NTR信号通路来实现对神经的再生修复。
引用
收藏
页码：1100 / 1106
页数：7
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