[1]陶广林,马善新,廖 媚.A型肉毒毒素应用于神经性疼痛的研究[J].医学信息,2020,33(09):24-28.[doi:10.3969/j.issn.1006-1959.2020.09.009]
 TAO Guang-lin,MA Shan-xin,LIAO Mei.Study on the Application of Botulinum Toxin A in Neuropathic Pain[J].Medical Information,2020,33(09):24-28.[doi:10.3969/j.issn.1006-1959.2020.09.009]
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A型肉毒毒素应用于神经性疼痛的研究()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
33卷
期数:
2020年09期
页码:
24-28
栏目:
综述
出版日期:
2020-05-01

文章信息/Info

Title:
Study on the Application of Botulinum Toxin A in Neuropathic Pain
文章编号:
1006-1959(2020)09-0024-06
作者:
陶广林马善新廖 媚
(1.广西医科大学第一附属医院康复医学科,广西 南宁 530021;2.深圳大学总医院康复医学科,广东 深圳 518055)
Author(s):
TAO Guang-linMA Shan-xinLIAO Mei
(1.Department of Rehabilitation Medicine,the First Affiliated Hospital of Guangxi Medical University,Nanning 530021,Guangxi,China;2.Department of Rehabilitation Medicine,Shenzhen University General Hospital,Shenzhen 518055,Guangdong,China)
关键词:
肉毒毒素神经性疼痛小胶质细胞神经元星型胶质细胞
Keywords:
Botulinum toxinNeuropathic painMicrogliaNeuronsAstrocytes
分类号:
R741
DOI:
10.3969/j.issn.1006-1959.2020.09.009
文献标志码:
A
摘要:
神经性疼痛是一种慢性疾病,治疗较难,是目前临床上比较棘手的问题。A型肉毒毒素(BTX-A)目前用于治疗与疼痛相关的各种临床疾病,其作用机制是阻断神经肌肉接头处的乙酰胆碱递质释放,指导突触连接的形成和细化。既往研究已证实BTX-A对突触小泡融合的抑制作用可以阻断其它疼痛相关神经传递素的释放。越来越多的证据表明,BTX-A的镇痛作用是通过神经元和胶质细胞介导的,尤其是小胶质细胞的介导作用,可通过减少在小胶质细胞中磷酸化的ERK1/2,NF-κB和p38直接与TLR2相互作用来发挥其抗炎效果。此外,BTX-A可能对星形胶质细胞的作用不大,需要通过小胶质细胞中的功能性TLR4来完全激活星形胶质细胞中TLR2的活性,并强调这两种细胞之间相互作用的重要性。本文现对BTX-A对脊髓神经胶质细胞之间的相互作用及神经病变的发展影响进行综述。
Abstract:
Neuropathic pain is a chronic disease that is difficult to treat and is currently a clinically difficult issue. Botulinum toxin type A (BTX-A) is currently used to treat various clinical diseases related to pain, and its mechanism of action is to block the release of acetylcholine transmitters at the neuromuscular junction and guide the formation and refinement of synaptic connections. Previous studies have confirmed that the inhibitory effect of BTX-A on synaptic vesicle fusion can block the release of other pain-related neurotransmitters. There is increasing evidence that the analgesic effect of BTX-A is mediated by neurons and glial cells, especially the microglial cells, by reducing phosphorylation in microglia ERK1/2, NF-κB and p38 directly interact with TLR2 to exert their anti-inflammatory effects. In addition, BTX-A may have little effect on astrocytes. It is necessary to fully activate the activity of TLR2 in astrocytes by functional TLR4 in microglia, and emphasize the mutual importance of the role interaction between these two cells. This article now reviews the effects of BTX-A on the interaction between spinal glial cells and the development of neuropathy.

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更新日期/Last Update: 2020-05-01