Low-Dose Taxol Promotes Neuronal Axons Extension and Functional Recovery after Spinal Cord Injury.
Low-Dose Taxol Promotes Neuronal Axons Extension and Functional Recovery after Spinal Cord Injury.
复制标题
低剂量紫杉醇促进脊髓损伤后神经元轴突延伸和功能恢复
DOI:
10.1155/2023/5604103
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发表时间:
2023
影响因子:
4.6
通讯作者:
Sun, Dejun
中科院分区:
文献类型:
--
作者:
Liu, Baoguo;Liu, Sumei;Sun, Dejun
Axonal regeneration has been the research focus in the field of clinical treatment for spinal cord injury (SCI). The growth and extension of neuronal axons is a dynamic biological process mediated by the cytoskeleton, and microtubule plays an important role in axonal growth. Moderate stabilization of microtubule promotes axonal growth and eliminates various intra- and extracellular mechanisms that impede axonal regeneration. After SCI, the damaged axons rapidly form a growth cone, wherein the stability of tubulin decreases, impairing axonal regeneration. Taxol with proven clinical safety is commonly used as a broad-spectrum antitumor drug. Importantly, Taxol can promote axonal extension by enhancing and stabilizing the microtubule assembly. In our study, we systematically investigated the differentiation of neural stem cells (NSCs) in vitro and functional recovery in injured rats in vivo following Taxol treatment. Low-dose Taxol promoted differentiation of NSCs to neurons and significantly extended the axons in vitro. In vivo, Taxol promoted the expression of βIII-tubulin in the injured areas and motor function recovery after SCI. Low-dose Taxol is a promising clinical agent to promote axonal regeneration after SCI.
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影响因子:
5.3
作者:
Fournier, AE;Takizawa, BT;Strittmatter, SM
通讯作者:
Strittmatter, SM
影响因子:
4.2
作者:
Soldati, Chiara;Caramanica, Pasquale;Cacci, Emanuele
通讯作者:
Cacci, Emanuele
DOI:
10.1196/annals.1377.013
发表时间:
2006-01-01
期刊:
INTEGRATED MOLECULAR MEDICINE FOR NEURONAL AND NEOPLASTIC DISORDERS
影响因子:
--
作者:
Yoshimura, Takeshi;Arimura, Nariko;Kaibuchi, Kozo
通讯作者:
Kaibuchi, Kozo
影响因子:
64.8
作者:
BENTLEY, D;TOROIANRAYMOND, A
通讯作者:
TOROIANRAYMOND, A
影响因子:
64.8
作者:
BAMBURG, JR;BRAY, D;CHAPMAN, K
通讯作者:
CHAPMAN, K