Evidence map›Paper›PMID 26978376›Full record

ArticleMarine drugs2016

Astaxanthin Inhibits Acetaldehyde-Induced Cytotoxicity in SH-SY5Y Cells by Modulating Akt/CREB and p38MAPK/ERK Signaling Pathways.

Tingting Yan, Yan Zhao, Xia Zhang, Xiaotong Lin

Open access · goldAbstract read
In one paragraph

Article in Marine drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-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

25 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Astaxanthin Inhibits HMarine drugs · 2024
    Article
  7. Protective effects ofFrontiers in microbiology · 2024
    Article
  8. Article
  9. Article
  10. Metabolites with Antioxidant Activity from Marine Macroalgae.Antioxidants (Basel, Switzerland) · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Melatonin Rescue Oxidative Stress-Mediated Neuroinflammation/ Neurodegeneration and Memory Impairment in Scopolamine-Induced Amnesia Mice Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Article
  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

4 authors at 1 institution in 1 country.

Tingting YanDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, Shandong, China. alovelong@aliyun.com.
Yan ZhaoDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, Shandong, China. zhaoyan@hitwh.edu.cn.
Xia ZhangDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, Shandong, China. zx080750106@163.com.
Xiaotong LinDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, Shandong, China. 18766312033@163.com.
Harbin Institute of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive alcohol consumption can lead to brain tissue damage and cognitive dysfunction. Acetaldehyde, the most toxic metabolite of ethanol, mediates the brain tissue damage and cognitive dysfunction induced by chronic excessive alcohol consumption. In this study, the effect of astaxanthin, a marine bioactive compound, on acetaldehyde-induced cytotoxicity was investigated in SH-SY5Y cells. It was found that astaxanthin protected cells from apoptosis by ameliorating the effect of acetaldehyde on the expression of Bcl-2 family proteins, preventing the reduction of anti-apoptotic protein Bcl-2 and the increase of pro-apoptotic protein Bak induced by acetaldehyde. Further analyses showed that astaxanthin treatment inhibited acetaldehyde-induced reduction of the levels of activated Akt and cyclic AMP-responsive element binding protein (CREB). Astaxanthin treatment also prevented acetaldehyde-induced increase of the level of activated p38 mitogen-activated protein kinase (MAPK) and decrease of the level of activated extracellular signal-regulated kinases (ERKs). Activation of Akt/CREB pathway promotes cell survival and is involved in the upregulation of Bcl-2 gene. P38MAPK plays a critical role in apoptotic events while ERKs mediates the inhibition of apoptosis. Thus, astaxanthin may inhibit acetaldehyde-induced apoptosis through promoting the activation of Akt/CREB and ERKs and blocking the activation of p38MAPK. In addition, astaxanthin treatment suppressed the oxidative stress induced by acetaldehyde and restored the antioxidative capacity of SH-SY5Y cells. Therefore, astaxanthin may protect cells against acetaldehyde-induced cytotoxicity through maintaining redox balance and modulating apoptotic and survival signals. The results suggest that astaxanthin treatment may be beneficial for preventing neurotoxicity associated with acetaldehyde and excessive alcohol consumption.

Indexed as

AcetaldehydeApoptosisCell Line, TumorCell SurvivalCyclic AMP Response Element-Binding ProteinExtracellular Signal-Regulated MAP KinasesGenes, bcl-2HumansNeurotoxicity SyndromesOxidative Stressp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktSignal TransductionUp-RegulationXanthophyllsAcetaldehydeastaxanthineCyclic AMP Response Element-Binding ProteinExtracellular Signal-Regulated MAP Kinasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktXanthophyllsacetaldehydeAktapoptosisastaxanthinMAPKoxidative stress

Identifiers

PMID26978376
PMCPMC4820310
OpenAlexW2296310309

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.