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本文引用的文献

1
The Temporal Pattern, Flux, and Function of Autophagy in Spinal Cord Injury.脊髓损伤中自噬的时间模式、通量及功能
Int J Mol Sci. 2017 Feb 21;18(2):466. doi: 10.3390/ijms18020466.
2
Autophagy Inhibition Favors Survival of Rubrospinal Neurons After Spinal Cord Hemisection.自噬抑制有利于脊髓半切后红核脊髓神经元的存活。
Mol Neurobiol. 2017 Sep;54(7):4896-4907. doi: 10.1007/s12035-016-0031-z. Epub 2016 Aug 11.
3
Protective Effects of Costunolide against Hydrogen Peroxide-Induced Injury in PC12 Cells.木香烯内酯对过氧化氢诱导的PC12细胞损伤的保护作用。
Molecules. 2016 Jul 9;21(7):898. doi: 10.3390/molecules21070898.
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Inhibition of Autophagy by Estradiol Promotes Locomotor Recovery after Spinal Cord Injury in Rats.雌二醇抑制自噬促进大鼠脊髓损伤后运动功能恢复
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5
Involvement of Connexin40 in the Protective Effects of Ginsenoside Rb1 Against Traumatic Brain Injury.连接蛋白40在人参皂苷Rb1对创伤性脑损伤的保护作用中的作用
Cell Mol Neurobiol. 2016 Oct;36(7):1057-65. doi: 10.1007/s10571-015-0299-y. Epub 2015 Dec 8.
6
Ginsenoside Rb1 Attenuates Acute Inflammatory Nociception by Inhibition of Neuronal ERK Phosphorylation by Regulation of the Nrf2 and NF-κB Pathways.人参皂苷Rb1通过调节Nrf2和NF-κB信号通路抑制神经元ERK磷酸化,从而减轻急性炎性疼痛。
J Pain. 2016 Mar;17(3):282-97. doi: 10.1016/j.jpain.2015.10.007. Epub 2015 Nov 6.
7
Rapamycin increases neuronal survival, reduces inflammation and astrocyte proliferation after spinal cord injury.雷帕霉素可提高脊髓损伤后神经元的存活率,减轻炎症反应并减少星形胶质细胞增殖。
Mol Cell Neurosci. 2015 Sep;68:82-91. doi: 10.1016/j.mcn.2015.04.006. Epub 2015 Apr 30.
8
Chaperone-Mediated Autophagy after Traumatic Brain Injury.创伤性脑损伤后的伴侣介导自噬
J Neurotrauma. 2015 Oct 1;32(19):1449-57. doi: 10.1089/neu.2014.3694. Epub 2015 Jun 30.
9
Korean Red Ginseng and Ginsenoside-Rb1/-Rg1 Alleviate Experimental Autoimmune Encephalomyelitis by Suppressing Th1 and Th17 Cells and Upregulating Regulatory T Cells.韩国红参及人参皂苷-Rb1/-Rg1通过抑制Th1和Th17细胞并上调调节性T细胞来减轻实验性自身免疫性脑脊髓炎。
Mol Neurobiol. 2016 Apr;53(3):1977-2002. doi: 10.1007/s12035-015-9131-4. Epub 2015 Apr 7.
10
Effects of Therapeutic Hypothermia on Apoptosis and Autophagy After Spinal Cord Injury in Rats.亚低温对大鼠脊髓损伤后细胞凋亡和自噬的影响
Spine (Phila Pa 1976). 2015 Jun 15;40(12):883-90. doi: 10.1097/BRS.0000000000000845.

自噬抑制参与人参皂苷 Rb1 对脊髓损伤的保护作用。

Inhibition of Autophagy is Involved in the Protective Effects of Ginsenoside Rb1 on Spinal Cord Injury.

机构信息

Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.

Institute of Neuroscience and Institute of Hypoxia Medicine, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.

出版信息

Cell Mol Neurobiol. 2018 Apr;38(3):679-690. doi: 10.1007/s10571-017-0527-8. Epub 2017 Jul 31.

DOI:10.1007/s10571-017-0527-8
PMID:28762191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11481967/
Abstract

Spinal cord injury (SCI) is a devastating neurological disorder. Autophagy is induced and plays a crucial role in SCI. Ginsenoside Rb1 (Rb1), one of the major active components extracted from Panax Ginseng CA Meyer, has exhibited neuroprotective effects in various neurodegenerative diseases. However, it remains unknown whether autophagy is involved in the neuroprotection of Rb1 on SCI. In this study, we examined the regulation of autophagy following Rb1 treatment and its involvement in the Rb1-induced neuroprotection in SCI and in vitro injury model. Firstly, we found that Rb1 treatment decreased the loss of motor neurons and promoted function recovery in the SCI model. Furthermore, we found that Rb1 treatment inhibited autophagy in neurons, and suppressed neuronal apoptosis and autophagic cell death in the SCI model. Finally, in the in vitro injury model, Rb1 treatment increased the viability of PC12 cells and suppressed apoptosis by inhibiting excessive autophagy, whereas stimulation of autophagy by rapamycin abolished the anti-apoptosis effect of Rb1. Taken together, these findings suggest that the inhibition of autophagy is involved in the neuroprotective effects of Rb1 on SCI.

摘要

脊髓损伤(SCI)是一种毁灭性的神经系统疾病。自噬被诱导并在 SCI 中发挥关键作用。人参皂苷 Rb1(Rb1)是从 Panax Ginseng CA Meyer 中提取的主要活性成分之一,在各种神经退行性疾病中表现出神经保护作用。然而,尚不清楚自噬是否参与 Rb1 对 SCI 的神经保护作用。在这项研究中,我们研究了 Rb1 处理后自噬的调节及其在 SCI 和体外损伤模型中 Rb1 诱导的神经保护作用中的参与。首先,我们发现 Rb1 处理可减少运动神经元的丢失并促进 SCI 模型中的功能恢复。此外,我们发现 Rb1 处理可抑制神经元中的自噬,并抑制 SCI 模型中的神经元凋亡和自噬性细胞死亡。最后,在体外损伤模型中,Rb1 处理通过抑制过度自噬增加 PC12 细胞的活力并抑制细胞凋亡,而雷帕霉素刺激自噬则消除了 Rb1 的抗细胞凋亡作用。综上所述,这些发现表明自噬的抑制参与了 Rb1 对 SCI 的神经保护作用。