• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

α-硫辛酸可改善 6-羟多巴胺诱导的帕金森病模型的运动缺陷和线粒体动力学。

Alpha Lipoamide Ameliorates Motor Deficits and Mitochondrial Dynamics in the Parkinson's Disease Model Induced by 6-Hydroxydopamine.

机构信息

State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guizhou, 550004, China.

Engineering Technology Research Center for Chemical Drug R&D, Guizhou, 550004, China.

出版信息

Neurotox Res. 2018 May;33(4):759-767. doi: 10.1007/s12640-017-9819-5. Epub 2017 Oct 10.

DOI:10.1007/s12640-017-9819-5
PMID:29019159
Abstract

The precise mechanisms underlying neuronal injury in Parkinson's disease (PD) are not yet fully elucidated; however, evidence from the in vitro and in vivo PD models suggest that mitochondrial dysfunction may play a major role in PD pathogenesis. Alpha lipoamide, a neutral amide derivative of the lipoic acid, is a better cofactor for mitochondrial dehydrogenase with a stronger protective effect on mitochondria than lipoic acid. Identification of these protective effects of alpha lipoamide on mitochondria, together with the evidence that mitochondrial dysfunction plays a critical role in PD, we speculate that alpha lipoamide may exert a protective effect in PD by regulating the mitochondrial function. The present study investigated the neuroprotective effects of alpha lipoamide in an animal model of PD induced by 6-hydroxydopamine (6-OHDA). The results demonstrated that alpha lipoamide could significantly antagonize the 6-OHDA-induced behavioral damages; restore ATP levels in the midbrain; and also improve the fragmentation, vacuolization, and morphology of the mitochondria. The results of Western blot indicated that alpha lipoamide significantly restored the number of dopaminergic neurons in midbrain and substantially recovered the balance between mitochondrial fission, fusion, and transport. In conclusion, the results demonstrated that alpha lipoamide might exert a significant neuroprotective effect in the animal model of PD by regulation of the dynamic properties of mitochondria.

摘要

帕金森病(PD)中神经元损伤的确切机制尚未完全阐明;然而,来自 PD 体外和体内模型的证据表明,线粒体功能障碍可能在 PD 发病机制中起主要作用。α-硫辛酸是硫辛酸的中性酰胺衍生物,是线粒体脱氢酶的更好辅助因子,对线粒体的保护作用比硫辛酸更强。鉴定α-硫辛酸对线粒体的这些保护作用,以及线粒体功能障碍在 PD 中起关键作用的证据,我们推测α-硫辛酸可能通过调节线粒体功能在 PD 中发挥保护作用。本研究探讨了α-硫辛酸在 6-羟多巴胺(6-OHDA)诱导的 PD 动物模型中的神经保护作用。结果表明,α-硫辛酸能显著拮抗 6-OHDA 引起的行为损伤;恢复中脑 ATP 水平;并改善线粒体的碎片化、空泡化和形态。Western blot 结果表明,α-硫辛酸可显著恢复中脑多巴胺能神经元的数量,并显著恢复线粒体分裂、融合和运输之间的平衡。总之,结果表明,α-硫辛酸可能通过调节线粒体的动态特性在 PD 动物模型中发挥显著的神经保护作用。

相似文献

1
Alpha Lipoamide Ameliorates Motor Deficits and Mitochondrial Dynamics in the Parkinson's Disease Model Induced by 6-Hydroxydopamine.α-硫辛酸可改善 6-羟多巴胺诱导的帕金森病模型的运动缺陷和线粒体动力学。
Neurotox Res. 2018 May;33(4):759-767. doi: 10.1007/s12640-017-9819-5. Epub 2017 Oct 10.
2
Dopamine D1 receptor agonism induces dynamin related protein-1 inhibition to improve mitochondrial biogenesis and dopaminergic neurogenesis in rat model of Parkinson's disease.多巴胺 D1 受体激动剂诱导动力相关蛋白 1 抑制以改善帕金森病大鼠模型中的线粒体生物发生和多巴胺能神经发生。
Behav Brain Res. 2020 Jan 27;378:112304. doi: 10.1016/j.bbr.2019.112304. Epub 2019 Oct 15.
3
Squamosamide derivative FLZ protected dopaminergic neuron by activating Akt signaling pathway in 6-OHDA-induced in vivo and in vitro Parkinson's disease models.鳞酰胺衍生物 FLZ 通过激活 Akt 信号通路在 6-OHDA 诱导的体内和体外帕金森病模型中保护多巴胺能神经元。
Brain Res. 2014 Feb 14;1547:49-57. doi: 10.1016/j.brainres.2013.12.026. Epub 2013 Dec 30.
4
MitoQ protects dopaminergic neurons in a 6-OHDA induced PD model by enhancing Mfn2-dependent mitochondrial fusion via activation of PGC-1α.MitoQ 通过激活 PGC-1α 增强 Mfn2 依赖性线粒体融合,从而保护 6-OHDA 诱导的 PD 模型中的多巴胺能神经元。
Biochim Biophys Acta Mol Basis Dis. 2018 Sep;1864(9 Pt B):2859-2870. doi: 10.1016/j.bbadis.2018.05.018. Epub 2018 May 26.
5
Evaluation of the antiparkinsonism and neuroprotective effects of hydrogen sulfide in acute 6-hydroxydopamine-induced animal model of Parkinson's disease: behavioral, histological and biochemical studies.硫化氢在急性6-羟基多巴胺诱导的帕金森病动物模型中的抗帕金森病及神经保护作用评估:行为学、组织学和生物化学研究
Neurol Res. 2018 Jul;40(7):523-531. doi: 10.1080/01616412.2017.1390903. Epub 2018 May 4.
6
Neuroprotective effects of neurokinin receptor one in dopaminergic neurons are mediated through Akt/PKB cell signaling pathway.神经激肽受体 1 对多巴胺能神经元的神经保护作用是通过 Akt/PKB 细胞信号通路介导的。
Neuropharmacology. 2011 Dec;61(8):1389-98. doi: 10.1016/j.neuropharm.2011.08.027. Epub 2011 Sep 3.
7
Neuroprotection by scorpion venom heat resistant peptide in 6-hydroxydopamine rat model of early-stage Parkinson's disease.蝎毒耐热肽对早期帕金森病6-羟基多巴胺大鼠模型的神经保护作用
Sheng Li Xue Bao. 2014 Dec 25;66(6):658-66.
8
Dopamine transporter-mediated cytotoxicity of 6-hydroxydopamine in vitro depends on expression of mutant alpha-synucleins related to Parkinson's disease.多巴胺转运体介导的6-羟基多巴胺体外细胞毒性取决于与帕金森病相关的突变α-突触核蛋白的表达。
Neurochem Int. 2006 Apr;48(5):329-40. doi: 10.1016/j.neuint.2005.11.008. Epub 2006 Jan 6.
9
Gender-specific role of mitochondria in the vulnerability of 6-hydroxydopamine-treated mesencephalic neurons.线粒体在6-羟基多巴胺处理的中脑神经元易损性中的性别特异性作用。
Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):1178-88. doi: 10.1016/j.bbabio.2010.04.009. Epub 2010 Apr 20.
10
FGF18 protects against 6-hydroxydopamine-induced nigrostriatal damage in a rat model of Parkinson's disease.在帕金森病大鼠模型中,成纤维细胞生长因子18可预防6-羟基多巴胺诱导的黑质纹状体损伤。
Neuroscience. 2017 Jul 25;356:229-241. doi: 10.1016/j.neuroscience.2017.05.007. Epub 2017 May 11.

引用本文的文献

1
Mitochondrial quality control disorder in neurodegenerative disorders: Potential and advantages of traditional Chinese medicines.神经退行性疾病中的线粒体质量控制紊乱:中药的潜力与优势
J Pharm Anal. 2025 Apr;15(4):101146. doi: 10.1016/j.jpha.2024.101146. Epub 2024 Nov 14.
2
A Multi-Target Pharmacological Correction of a Lipoyltransferase Gene Mutation in Patient-Derived Cellular Models.患者来源细胞模型中硫辛酰转移酶基因突变的多靶点药理学校正
Antioxidants (Basel). 2024 Aug 22;13(8):1023. doi: 10.3390/antiox13081023.
3
Lipoamide Attenuates Hypertensive Myocardial Hypertrophy Through PI3K/Akt-Mediated Nrf2 Signaling Pathway.

本文引用的文献

1
Mitochondrial fission and fusion.线粒体分裂与融合
Biochem Soc Trans. 2016 Dec 15;44(6):1725-1735. doi: 10.1042/BST20160129.
2
Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment.神经退行性疾病中的线粒体功能障碍与生物发生:发病机制与治疗
CNS Neurosci Ther. 2017 Jan;23(1):5-22. doi: 10.1111/cns.12655. Epub 2016 Nov 22.
3
Dysregulation of autophagy and mitochondrial function in Parkinson's disease.帕金森病中自噬与线粒体功能的失调
脂酰基辅酶 A 减弱高血压心肌肥厚通过 PI3K/Akt 介导的 Nrf2 信号通路。
J Cardiovasc Transl Res. 2024 Aug;17(4):910-922. doi: 10.1007/s12265-024-10488-9. Epub 2024 Feb 9.
4
Alpha lipoamide inhibits diabetic kidney fibrosis via improving mitochondrial function and regulating RXRα expression and activation.α-硫辛酸通过改善线粒体功能和调节 RXRα 的表达和激活抑制糖尿病肾病纤维化。
Acta Pharmacol Sin. 2023 May;44(5):1051-1065. doi: 10.1038/s41401-022-00997-1. Epub 2022 Nov 8.
5
Lipoamide Alleviates Oxidized Fish Oil-Induced Host Inflammatory Response and Oxidative Damage in the Oviduct of Laying Hens.硫辛酸减轻氧化鱼油诱导的蛋鸡输卵管宿主炎症反应和氧化损伤。
Front Vet Sci. 2022 Apr 4;9:875769. doi: 10.3389/fvets.2022.875769. eCollection 2022.
6
Squamosamide Derivative FLZ Diminishes Aberrant Mitochondrial Fission by Inhibiting Dynamin-Related Protein 1.鳞状酰胺衍生物FLZ通过抑制动力相关蛋白1减少异常线粒体分裂。
Front Pharmacol. 2021 Mar 19;12:588003. doi: 10.3389/fphar.2021.588003. eCollection 2021.
7
Oxidative Stress in Parkinson's Disease: Potential Benefits of Antioxidant Supplementation.帕金森病中的氧化应激:抗氧化补充剂的潜在益处。
Oxid Med Cell Longev. 2020 Oct 12;2020:2360872. doi: 10.1155/2020/2360872. eCollection 2020.
8
Alpha-Lipoic Acid Mediates Clearance of Iron Accumulation by Regulating Iron Metabolism in a Parkinson's Disease Model Induced by 6-OHDA.α-硫辛酸通过调节6-羟基多巴胺诱导的帕金森病模型中的铁代谢来介导铁蓄积的清除。
Front Neurosci. 2020 Jun 25;14:612. doi: 10.3389/fnins.2020.00612. eCollection 2020.
9
Genetic Defects in Mitochondrial Dynamics in Impact Ultraviolet C Radiation- and 6-hydroxydopamine-Induced Neurodegeneration.线粒体动态遗传缺陷在紫外线 C 辐射和 6-羟多巴胺诱导的神经退行性变中的作用。
Int J Mol Sci. 2019 Jun 29;20(13):3202. doi: 10.3390/ijms20133202.
10
Da-Bu-Yin-Wan and Qian-Zheng-San Ameliorate Mitochondrial Dynamics in the Parkinson's Disease Cell Model Induced by MPP.大补阴丸和牵正散改善MPP诱导的帕金森病细胞模型中的线粒体动力学。
Front Pharmacol. 2019 Apr 24;10:372. doi: 10.3389/fphar.2019.00372. eCollection 2019.
Transl Neurodegener. 2016 Oct 31;5:19. doi: 10.1186/s40035-016-0065-1. eCollection 2016.
4
Mitochondrial dysfunction in Parkinson's disease.帕金森病中的线粒体功能障碍
Transl Neurodegener. 2016 Jul 22;5:14. doi: 10.1186/s40035-016-0060-6. eCollection 2016.
5
Live imaging of mitochondrial dynamics in CNS dopaminergic neurons in vivo demonstrates early reversal of mitochondrial transport following MPP(+) exposure.对体内中枢神经系统多巴胺能神经元中线粒体动力学的实时成像显示,暴露于MPP(+)后线粒体运输早期出现逆转。
Neurobiol Dis. 2016 Nov;95:238-49. doi: 10.1016/j.nbd.2016.07.020. Epub 2016 Jul 22.
6
Neuroprotective and Therapeutic Strategies against Parkinson's Disease: Recent Perspectives.帕金森病的神经保护与治疗策略:最新观点
Int J Mol Sci. 2016 Jun 8;17(6):904. doi: 10.3390/ijms17060904.
7
The Interaction of Mitochondrial Biogenesis and Fission/Fusion Mediated by PGC-1α Regulates Rotenone-Induced Dopaminergic Neurotoxicity.由PGC-1α介导的线粒体生物合成与分裂/融合的相互作用调节鱼藤酮诱导的多巴胺能神经毒性。
Mol Neurobiol. 2017 Jul;54(5):3783-3797. doi: 10.1007/s12035-016-9944-9. Epub 2016 Jun 7.
8
Parkinson's disease-associated mutant VPS35 causes mitochondrial dysfunction by recycling DLP1 complexes.帕金森病相关突变体VPS35通过回收动力蛋白1复合物导致线粒体功能障碍。
Nat Med. 2016 Jan;22(1):54-63. doi: 10.1038/nm.3983. Epub 2015 Nov 30.
9
Understanding the susceptibility of dopamine neurons to mitochondrial stressors in Parkinson's disease.了解帕金森病中多巴胺能神经元对线粒体应激源的易感性。
FEBS Lett. 2015 Dec 21;589(24 Pt A):3702-13. doi: 10.1016/j.febslet.2015.10.021. Epub 2015 Oct 23.
10
Mitochondrial fusion/fission dynamics in neurodegeneration and neuronal plasticity.线粒体融合/裂变动力学在神经变性和神经元可塑性中的作用。
Neurobiol Dis. 2016 Jun;90:3-19. doi: 10.1016/j.nbd.2015.10.011. Epub 2015 Oct 19.