Evidence map›Paper›PMID 25360664›Full record

ArticlePloS one2014

Methyllycaconitine alleviates amyloid-β peptides-induced cytotoxicity in SH-SY5Y cells.

XiaoLei Zheng, ZhaoHong Xie, ZhengYu Zhu, Zhen Liu, Yun Wang, LiFei Wei, Hui Yang, HongNa Yang, YiQing Liu, JianZhong Bi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Frontiers in microbiology · 2026
    Article
  2. Article
  3. Article
  4. Neuropharmacological Potential of Diterpenoid Alkaloids.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  5. Article
  6. VANL-100 Attenuates Beta-Amyloid-Induced Toxicity in SH-SY5Y Cells.International journal of molecular sciences · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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  14. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

XiaoLei ZhengDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
ZhaoHong XieDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
ZhengYu ZhuDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
Zhen LiuDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
Yun WangDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
LiFei WeiDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
Hui YangDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
HongNa YangDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
YiQing LiuDepartment of Neural Medicine, Second Hospital of Shandong University, Jinan, China.
JianZhong BiDepartment 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.
Second Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AconitineAmyloid beta-PeptidesAutophagyCell Line, TumorCell ProliferationHumansPeptide FragmentsSignal TransductionTOR Serine-Threonine KinasesAconitineAmyloid beta-Peptidesamyloid beta-protein (25-35)methyllycaconitinePeptide FragmentsTOR Serine-Threonine Kinases

Identifiers

PMID25360664
PMCPMC4216102
OpenAlexW2079010524

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.