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艾塞那肽对神经退行性疾病治疗作用的研究进展

Advances of the treatment of exendin-4 on neurodegenerative diseases
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摘要 艾塞那肽(exendin-4,Ex-4)作为一种胰高血糖素样肽-1(glucagon-like peptide-1,GLP-1)受体激动剂,主要作用于胰腺和胃肠道中的GLP-1受体以调节血糖水平,因此在2型糖尿病治疗中至关重要。研究表明,Ex-4可透过血脑屏障作用于脑内GLP-1受体,通过多种机制发挥神经保护作用。然而,药物疗效与疾病阶段的关系以及长期使用的安全性仍需进一步验证。尽管如此,该药物在神经退行性疾病治疗方面的潜力仍受关注。本文重点阐述了艾塞那肽在衰老相关神经退行性疾病治疗作用的最新进展。 As an agonist for the glucagon-like peptide-1(GLP-1)receptor,exendin-4(Ex-4)primarily targets GLP-1 receptors in the pancreas and gastrointestinal tract.Ex-4 is essential in the treatment of type 2 diabetes.It has been reported that Ex-4 can cross the blood-brain barrier and act on GLP-1 receptors in the brain,exerting neuroprotective effects through various mechanisms.However,the efficacy of the drug in relation to the stage of the disease,as well as the safety issues of longterm use still need to be further verified.Nevertheless,the potential of this drug in the treatment of neurodegenerative diseases is still under scrutiny.The present review highlights the latest advancements in the use of exendin-4 for treating age-related neurodegenerative diseases.
作者 苏小慧 鱼帆 宋新雅 杨好 周杰 丁小涵 SU Xiaohui;YU Fan;SONG Xinya;YANG Hao;ZHOU Jie;DING Xiaohan(Department One of the Healthcare Section,the 940th Hospital of Joint Logistics Support Force of Chinese PLA,Lanzhou,Gansu 730050,China;Department of Neurosurgery,the 940th Hospital of Joint Logistics Support Force of Chinese PLA,Lanzhou,Gansu 730050,China)
出处 《中华神经外科疾病研究杂志》 2025年第5期180-186,共7页 Chinese Journal of Neurosurgical Disease Research
基金 军队保健课题(21BJZ42,2021yxky030) 兰州市科技局科技计划项目(2023-ZD-167)。
关键词 艾塞那肽 GLP-1类似物 衰老 神经退行性改变 阿尔兹海默症 exendin-4 GLP-1 agonist aging neurodegenerative changes alzheimer's disease
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  • 1Steffan JS, Agrawal N, Pallos J, Rockabrand E, Trotman LC, Slepko N, et al. SUMO modification of Huntingtin and Huntington's disease pathology. Science 2004, 304 (5667): 100- 104.
  • 2Wellington CL, Singaraja R, Ellerby L, Savill J, Roy S, Leavitt B, et al. Inhibiting caspase cleavage of huntingtin reduces toxicity and aggregate formation in neuronal and nonneuronal cells. J Biol Chem 2000, 275 (26): 19831-19838.
  • 3DiFiglia M, Sapp E, Chase KO, Davies SW, Bates GP, Vonsattel JP, et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. Science 1997, 277 (5334): 1990-1993.
  • 4Kegel KB, Sapp E, Yoder J, Cuiffo B, Sobin L, Kim YJ, et al. Huntingtin associates with acidic phospholipids at the plasma membrane. J Biol Cbem 2005, 280 (43): 36464-36473.
  • 5Humbert S, Bryson EA, Cordelieres FP, Connors NC, Datta SR, Finkbeiner S, et al. The IGF-1/Akt pathway is neuroprotective in Huntington's disease and involves Huntingtin phosphorylation by Akt. Dev Cell 2002, 2 (6): 831-837.
  • 6Warby SC, Chan EY, Metzler M, Gan L, Singaraja RR, Crocker SF, et al. Huntingtin phosphorylation on serine 421 is significantly reduced in the striatum and by polyglutamine expansion in vivo. Hum Mol Genet 2005, 14 (11): 1569-1577.
  • 7Dorval V, Fraser PE. SUMO on the road to neurodegeneration. Biochim Biophys Acta 2007, 1773 (6): 694-706.
  • 8Dohmen RJ. SUMO protein modification. Biochim Biophys Acta 2004, 1695 (1-3): 113-131.
  • 9Su HL, Li SS. Molecular features of human ubiquitin-like SUMO genes and their encoded proteins. Gene 2002, 296 (1-2): 65-73.
  • 10Hay RT. SUMO: a history of modification. Mol Cell 2005, 18(1): 1-12.

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