Evidence map›Paper›PMID 33036367›Full record

ArticleMolecules (Basel, Switzerland)2020

A Bibenzyl Component Moscatilin Mitigates Glycation-Mediated Damages in an SH-SY5Y Cell Model of Neurodegenerative Diseases through AMPK Activation and RAGE/NF-

Mei Chou Lai, Wayne Young Liu, Shorong-Shii Liou, I-Min Liu

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Biological Characteristics of a Novel Bibenzyl Synthase (Molecules (Basel, Switzerland) · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Chemical Constituents and Hypoglycemic Mechanisms ofMolecules (Basel, Switzerland) · 2023
    Article
  10. Review
  11. 3 Biotech · 2022
    Article
  12. Review
  13. Biological Activities of Natural Products.Molecules (Basel, Switzerland) · 2020
    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

4 authors at 2 institutions in 1 country.

Mei Chou LaiDepartment of Pharmacy and Master Program, Collage of Pharmacy and Health Care, Tajen University, Pingtung County 90741, Taiwan.
Wayne Young LiuDepartment of Urology, Jen-Ai Hospital, Taichung 41265, Taiwan.
Shorong-Shii LiouDepartment of Pharmacy and Master Program, Collage of Pharmacy and Health Care, Tajen University, Pingtung County 90741, Taiwan.
I-Min LiuDepartment of Pharmacy and Master Program, Collage of Pharmacy and Health Care, Tajen University, Pingtung County 90741, Taiwan.
Tajen University · TWJen-Ai Hospital · TW

Funding

Ministry of Science and Technology of Taiwan MOST 109-2320-B-127-001
6 · The paper itself

Abstract

Moscatilin can protect rat pheochromocytoma cells against methylglyoxal-induced damage. Elimination of the effect of advanced glycation end-products (AGEs) but activation of AMP-activated protein kinase (AMPK) are the potential therapeutic targets for the neurodegenerative diseases. Our study aimed to clarify AMPK signaling's role in the beneficial effects of moscatilin on the diabetic/hyperglycemia-associated neurodegenerative disorders. AGEs-induced injury in SH-SY5Y cells was used as an in vitro neurodegenerative model. AGEs stimulation resulted in cellular viability loss and reactive oxygen species production, and mitochondrial membrane potential collapse. It was observed that the cleaved forms of caspase-9, caspase-3, and poly (ADP-ribose) polymerase increased in SH-SY5Y cells following AGEs exposure. AGEs decreased Bcl-2 but increased Bax and p53 expression and nuclear factor kappa-B activation in SH-SY5Y cells. AGEs also attenuated the phosphorylation level of AMPK. These AGEs-induced detrimental effects were ameliorated by moscatilin, which was similar to the actions of metformin. Compound C, an inhibitor of AMPK, abolished the beneficial effects of moscatilin on the regulation of SH-SY5Y cells' function, indicating the involvement of AMPK. In conclusion, moscatilin offers a promising therapeutic strategy to reduce the neurotoxicity or AMPK dysfunction of AGEs. It provides a potential beneficial effect with AGEs-related neurodegenerative diseases.

Indexed as

Adenosine DiphosphateAdenosine TriphosphateAMP-Activated Protein KinasesBenzyl CompoundsBlotting, WesternCell SurvivalDNA FragmentationGlutathioneGlycation End Products, AdvancedHumansLipid PeroxidationMembrane Potential, MitochondrialNeurodegenerative DiseasesNF-kappa BOxidative StressReactive Oxygen SpeciesAdenosine DiphosphateAdenosine TriphosphateAMP-Activated Protein KinasesBenzyl CompoundsdendrophenolGlutathioneGlycation End Products, AdvancedNF-kappa BReactive Oxygen SpeciesReceptor for Advanced Glycation End Productsadvanced glycation end-productsAMP-activated protein kinasemoscatilinneurodegenerative diseasesSH-SY5Y cells

Identifiers

PMID33036367
PMCPMC7582731
OpenAlexW3091951800

What OpenQuestion holds

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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.