中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (10): 2026-2027.doi: 10.4103/1673-5374.308085

• 观点:退行性病与再生 • 上一篇    下一篇

海藻糖在神经退行性疾病中的治疗潜力:已知与未知

  

  • 出版日期:2021-10-15 发布日期:2021-03-19

Therapeutic potential of trehalose in neurodegenerative diseases: the knowns and unknowns

Masoomeh Khalifeh, George E. Barreto, Amirhossein Sahebkar*   

  1. Department of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran (Khalifeh M)
    Department of Biological Sciences; Health Research Institute, University of Limerick, Limerick, Ireland (Barreto GE)
    Applied Biomedical Research Center; Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran (Sahebkar A)
    Polish Mother’s Memorial Hospital Research Institute (PMMHRI), Lodz, Poland (Sahebkar A)
    School of Pharmacy Mashhad University of Medical Sciences, Mashhad, Iran (Sahebkar A)
  • Online:2021-10-15 Published:2021-03-19
  • Contact: Amirhossein Sahebkar, PharmD, PhD, sahebkara@mums.ac.ir or amir_saheb2000@yahoo.com.

摘要:

Neural Regen Res:海藻糖:治疗神经退行性疾病的有力候选药物

 

海藻糖被证实在各种神经退行性疾病(NDs)(例如帕金森病,阿尔茨海默病和亨廷舞蹈病)的动物模型中都具有神经保护作用。海藻糖,也被叫做mycose,是一种非还原性二糖,由两个葡萄糖分子组成,大量存在于微生物、植物和无脊椎动物中。海藻糖的物理和化学特性来自其非还原性,这导致其化学稳定性、高亲水性以及对酸水解和葡糖苷酶裂解的强抵抗力。摄入海藻糖作为饮食的一部分通常是安全的,不会引起血糖的快速升高。在最大剂量为50 g的情况下,海藻糖对人体是安全的。除海藻糖缺乏者外,大多数受试者没有任何症状,但可能会出现胃肠副作用。在动物研究中,尽管偶尔出现腹泻,但静脉给药后未见动物死亡。越来越多的证据表明海藻糖在NDs中的治疗潜力,并且作为安全物质在药物制剂(包括肠胃外产品)中被FDA广泛使用。

 

来自伊朗马什哈德医科大学的Amirhossein Sahebkar团队认为海藻糖的安全性能够促进相关药物进行进一步的临床试验研究。当在ND出现广泛的神经变性之前,海藻糖似乎起着更显著的作用。除治疗时机外,海藻糖正确剂量和给药途径也是非常重要的。海藻糖的神经保护作用是否遵循剂量依赖性模式仍是未知的。此外,与口服相比,静脉给药能够提高海藻糖的生物利用度,但是肠道菌群是否在海藻糖的神经保护作用中起主要作用仍不清楚。未来需要进一步探讨海藻糖的直接或间接给药是否引发脑功能的改变。

 

文章在《中国神经再生研究(英文版)》杂志20211010期发表。

https://orcid.org/0000-0002-8656-1444 (Amirhossein Sahebkar)

Abstract: Neurodegenerative diseases (NDs) are a growing health problem associated with a high burden due to destructive and long-term clinical effects. Cellular aggregations of misfolded proteins are the most common pathological hallmark of many late-onset NDs called proteinopathies including Parkinson’s disease (PD), Alzheimer’s disease (AD), tauopathies, amyotrophic lateral sclerosis (ALS), and polyglutamine (polyQ) expansion diseases such as Huntington’s disease (HD) and various spinocerebellar ataxias (SCA) such as SCA3 (Renna et al., 2010). Misfolded proteins can be generated by posttranslational conjugation (e.g., hyperphosphorylated tau in AD), or endoproteolytic cleavage (e.g., amyloid β peptides) or genetic mutations in specific proteins (such as HTT in HD, α-synuclein in PD, PrPC in prion disease and SOD1 and TDP-43 in ALS) leading to the formation of oligomers.