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本文引用的文献

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Systematic Review of Pharmacological Properties of the Oligodendrocyte Lineage.少突胶质细胞谱系药理特性的系统评价
Front Cell Neurosci. 2016 Feb 12;10:27. doi: 10.3389/fncel.2016.00027. eCollection 2016.
2
Both endoplasmic reticulum and mitochondrial pathways are involved in oligodendrocyte apoptosis induced by capsular hemorrhage.内质网和线粒体途径均参与了包膜下出血诱导的少突胶质细胞凋亡。
Mol Cell Neurosci. 2016 Apr;72:64-71. doi: 10.1016/j.mcn.2016.01.009. Epub 2016 Jan 22.
3
Fibroblast Growth Factor-2 Enhanced The Recruitment of Progenitor Cells and Myelin Repair in Experimental Demyelination of Rat Hippocampal Formations.成纤维细胞生长因子-2增强了大鼠海马结构实验性脱髓鞘中祖细胞的募集和髓鞘修复。
Cell J. 2015 Fall;17(3):540-456. doi: 10.22074/cellj.2015.14. Epub 2015 Oct 7.
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Myelin damage and repair in pathologic CNS: challenges and prospects.病理性中枢神经系统中的髓鞘损伤与修复:挑战与前景
Front Mol Neurosci. 2015 Jul 27;8:35. doi: 10.3389/fnmol.2015.00035. eCollection 2015.
5
Aggregation of MBP in chronic demyelination.髓鞘碱性蛋白在慢性脱髓鞘中的聚集。
Ann Clin Transl Neurol. 2015 Jul;2(7):711-21. doi: 10.1002/acn3.207. Epub 2015 Jun 6.
6
Developing traditional chinese medicine in the era of evidence-based medicine: current evidences and challenges.在循证医学时代发展中医药:当前证据与挑战。
Evid Based Complement Alternat Med. 2015;2015:425037. doi: 10.1155/2015/425037. Epub 2015 Apr 8.
7
Tamoxifen and Src kinase inhibitors as neuroprotective/neuroregenerative drugs after spinal cord injury.他莫昔芬和Src激酶抑制剂作为脊髓损伤后的神经保护/神经再生药物。
Neural Regen Res. 2015 Mar;10(3):385-90. doi: 10.4103/1673-5374.153685.
8
Honokiol downregulates Kruppel-like factor 4 expression, attenuates inflammation, and reduces histopathology after spinal cord injury in rats.厚朴酚可下调大鼠脊髓损伤后 Kruppel 样因子 4 的表达,减轻炎症反应,并减轻组织病理学损伤。
Spine (Phila Pa 1976). 2015 Mar 15;40(6):363-8. doi: 10.1097/BRS.0000000000000758.
9
Nonpeptide neurotrophic agents useful in the treatment of neurodegenerative diseases such as Alzheimer's disease.可用于治疗诸如阿尔茨海默病等神经退行性疾病的非肽神经营养剂。
J Pharmacol Sci. 2015 Feb;127(2):155-63. doi: 10.1016/j.jphs.2014.12.015. Epub 2015 Jan 13.
10
Function of microglia and macrophages in secondary damage after spinal cord injury.小胶质细胞和巨噬细胞在脊髓损伤后继发性损伤中的作用。
Neural Regen Res. 2014 Oct 15;9(20):1787-95. doi: 10.4103/1673-5374.143423.

霍诺酚醇通过调节内质网-线粒体相互作用抑制少突胶质细胞凋亡,对受压脊髓损伤后的神经髓鞘发挥保护作用。

Honokiol exerts protective effects on neural myelin sheaths after compressed spinal cord injury by inhibiting oligodendrocyte apoptosis through regulation of ER-mitochondrial interactions.

机构信息

Medical College, China Three Gorges University, Yichang, Hubei, People's Republic of China.

Institute of Neuroscience, Chongqing Medical University, Chongqing, People's Republic of China.

出版信息

J Spinal Cord Med. 2022 Jul;45(4):595-604. doi: 10.1080/10790268.2021.1890878. Epub 2021 Apr 8.

DOI:10.1080/10790268.2021.1890878
PMID:33830903
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9246194/
Abstract

OBJECTIVE

To investigate the effect of honokiol on demyelination after compressed spinal cord injury (CSCI) and it's possible mechanism.

DESIGN

Animal experiment study.

SETTING

Institute of Neuroscience of Chongqing Medical University.

INTERVENTIONS

Total of 69 Sprague-Dawley (SD) rats were randomly divided into 3 groups: sham group (n=15), honokiol group (n=27) and vehicle group (n=27). After established CSCI model by a custom-made compressor successfully, the rats of sham group were subjected to the limited laminectomy without compression; the rats of honokiol group were subjected to CSCI surgery and intraperitoneal injection of 20 mg/kg honokiol; the rats of vehicle group were subjected to CSCI surgery and intraperitoneal injection of an equivalent volume of saline. The locomotor function of each group was assessed using the Basso, Beattie and Bresnahan (BBB) rating scale. The pathological changes of myelinated nerve fibers of spinal cord in 3 groups were detected by osmic acid staining and transmission electron microcopy (TME). Immunofluorescence and Western blot were used to research the experessions of active caspase-3, caspase-12, cytochrome C and myelin basic protein (MBP) respectively.

RESULTS

In the vehicle group, the rats became paralyzed and spastic after injury, and the myelin sheath became swollen and broken down along with decreased number of myelinated nerve fibers. Western blot analysis manifested that active caspase-3, caspase-12 and cytochrome C began to increase 1 d after injury while the expression of MBP decreased gradually. After intervened with honokiol for 6 days, compared with the vehicle group, the locomotor function and the pathomorphological changes of myelin sheath of the CSCD rats were improved with obviously decreased expression of active caspase-3, caspase-12 and cytochrome C.

CONCLUSIONS

Honokiol may improve locomotor function and protect neural myelin sheat from demyelination via prevention oligodendrocytes (OLs) apoptosis through mediate endoplasmic reticulum (ER)-mitochondria pathway after CSCI.

摘要

目的

研究和厚朴酚对压迫性脊髓损伤后脱髓鞘的影响及其可能的机制。

设计

动物实验研究。

地点

重庆医科大学神经科学研究所。

干预

共 69 只 SD 大鼠随机分为 3 组:假手术组(n=15)、和厚朴酚组(n=27)和载体组(n=27)。成功建立定制压缩机致 CSCI 模型后,假手术组仅行有限椎板切除术而不压迫;和厚朴酚组行 CSCI 手术并腹腔内注射 20mg/kg 和厚朴酚;载体组行 CSCI 手术并腹腔内注射等容量生理盐水。采用 Basso、Beattie 和 Bresnahan(BBB)评分量表评估各组大鼠的运动功能。采用锇酸染色和透射电镜(TEM)检测 3 组脊髓有髓神经纤维的病理变化。免疫荧光和 Western blot 分别用于研究活性 caspase-3、caspase-12、细胞色素 C 和髓鞘碱性蛋白(MBP)的表达。

结果

载体组大鼠损伤后瘫痪痉挛,髓鞘肿胀断裂,有髓神经纤维数量减少。Western blot 分析表明,损伤后 1d 活性 caspase-3、caspase-12 和细胞色素 C 开始增加,MBP 表达逐渐减少。用和厚朴酚干预 6 天后,与载体组相比,CSCD 大鼠的运动功能和髓鞘病理变化得到改善,活性 caspase-3、caspase-12 和细胞色素 C 的表达明显降低。

结论

和厚朴酚可能通过介导内质网-线粒体途径抑制少突胶质细胞(OLs)凋亡,改善压迫性脊髓损伤后运动功能,保护神经髓鞘脱髓鞘。