Evidence map›Paper›PMID 27112440›Full record

ArticleJournal of molecular neuroscience : MN2016

Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1-42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1-42)-Injected Mice.

Meng Li, Sumin Qian

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Neuropharmacological effects ofFrontiers in neurology · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Gastrodin: a comprehensive pharmacological review.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  11. Article
  12. Article
  13. Review on pharmacological effects of gastrodin.Archives of pharmacal research · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Gastrodin and Vascular Dementia: Advances and Current Perspectives.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  18. Article
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Meng LiFifth Department of Neurology, Cangzhou Central Hospital, No. 16 Xinhua Western Road, Cangzhou, Hebei Province, 061000, China. dr.limeng@outlook.com.
Sumin QianSecond Department of Gynecology, Cangzhou Central Hospital, No. 16 Xinhua Western Road, Cangzhou, Hebei Province, 061000, China.
Cangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1-42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1-42) but also counteracts Aβ (1-42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1-42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1-42) exposure. Furthermore, in Aβ (1-42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1-42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1-42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1-42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer's disease.

Indexed as

NeurogenesisAmyloid beta-PeptidesAnimalsApoptosisBenzyl AlcoholsCell Line, TumorCells, CulturedCytokinesDoublecortin Domain ProteinsDoublecortin ProteinGlucosidesHippocampusHumansMiceMice, Inbred C57BLMicrotubule-Associated ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Benzyl AlcoholsCytokinesDCX protein, humanDcx protein, mouseDoublecortin Domain ProteinsDoublecortin ProteingastrodinGlucosidesMicrotubule-Associated ProteinsMitogen-Activated Protein KinasesNeuropeptidesNeuroprotective AgentsNitric OxidePeptide FragmentsSox2 protein, mouseSOXB1 Transcription FactorsAmyloid β (1–42)GastrodinHippocampal neurogenesisNeural progenitor cells

Identifiers

PMID27112440
OpenAlexW2343604687

What OpenQuestion holds

Textmetadata
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.