title: Methyllycaconitine alleviates amyloid-β peptides-induced cytotoxicity in SH-SY5Y cells.
abstract: Alzheimer's disease (AD) is a chronic progressive neurodegenerative disorder. As the most common form of dementia, it affects more than 35 million people worldwide and is increasing. Excessive extracellular deposition of amyloid-β peptide (Aβ) is a pathologic feature of AD. Accumulating evidence indicates that macroautophagy is involved in the pathogenesis of AD, but its exact role is still unclear. Although major findings on the molecular mechanisms have been reported, there are still no effective treatments to prevent, halt, or reverse Alzheimer's disease. In this study, we investigated whether Aβ25-35 could trigger an autophagy process and inhibit the growth of SH-SY5Y cells. Furthermore, we examined the effect of methyllycaconitine (MLA) on the cytotoxity of Aβ25-35. MLA had a protective effect against cytotoxity of Aβ, which may be related to its inhibition of Aβ-induced autophagy and the involvement of the mammalian target of rapamycin pathway. Moreover, MLA had a good safety profile. MLA treatment may be a promising therapeutic tool for AD.
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: XiaoLei
authors.initials: X
authors.lastname: Zheng
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: ZhaoHong
authors.initials: Z
authors.lastname: Xie
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: ZhengYu
authors.initials: Z
authors.lastname: Zhu
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Liu
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: LiFei
authors.initials: L
authors.lastname: Wei
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Yang
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: HongNa
authors.initials: H
authors.lastname: Yang
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
authors.forename: YiQing
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Neural Medicine, Second Hospital of Shandong University, Jinan, China; Institute of Neurology, Shandong University, Jinan, China; Key Laboratory of Translational Medicine on Neurological Degenerative Disease in Universities of Shandong (Shandong University), Jinan, China.
authors.forename: JianZhong
authors.initials: J
authors.lastname: Bi
mesh_terms: D000157:Aconitine / Q000031:analogs & derivatives* / Q000494:pharmacology; D016229:Amyloid beta-Peptides / Q000633:toxicity*; D001343:Autophagy / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D006801:Humans; D010446:Peptide Fragments / Q000633:toxicity*; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35); C054634:methyllycaconitine; D058570:TOR Serine-Threonine Kinases; D000157:Aconitine