Evidence map›Paper›PMID 27511125›Full record

ArticleInternational journal of molecular medicine2016

Neuroprotective effects of sodium hydrosulfide against β-amyloid-induced neurotoxicity.

Xiao-Hui Li, Yuan-Yuan Deng, Fei Li, Jing-Shan Shi, Qi-Hai Gong

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Protective Effect of Buyang Huanwu Decoction on Neurovascular Unit in Alzheimer's Disease Cell Model via Inflammation and RAGE/LRP1 Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  5. Involvement of Endothelin-1, HCellular and molecular neurobiology · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Protective Effects of Wogonin against Alzheimer's Disease by Inhibition of Amyloidogenic Pathway.Evidence-based complementary and alternative medicine : eCAM · 2017
    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

5 authors at 1 institution in 1 country.

Xiao-Hui LiDepartment of Pharmacology and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Yuan-Yuan DengDepartment of Pharmacology and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Fei LiDepartment of Pharmacology and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Jing-Shan ShiDepartment of Pharmacology and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Qi-Hai GongDepartment of Pharmacology and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
Zunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is known to be caused by the accumulation of amyloid-β peptide (Aβ). The accumulation of Aβ has been shown to cause learning and memory impairment in rats, and it has been shown that hydrogen sulfide donors, such as sodium hydrosulfide (NaHS) can attenuate these effects. However, the underlying mechanisms have not yet been fully eludicated. This study was designed to investigate whether NaHS attenuates the inflammation and apoptosis induced by Aβ. We demonstrated that NaHS attenuated Aβ25‑35-induced neuronal reduction and apoptosis, and inhibited the activation of pro-caspase-3. It also decreased the protein expresion of phosphodiesterase 5 (PDE5) in the hippocampus of the rats. In addition, NaHS upregulated the expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ, but it did not affect the expression of PPAR-β. Moreover, the Aβ25‑35‑exposed rats exhibited a decrease in IκB-α degradation and an increase in nuclear factor-κB (NF-κB) p65 phosphorylation levels, whereas these effects were attenuated by NaHS. Our data suggest that NaHS prevents Aβ-induced neurotoxicity via the upregulation of PPAR-α and PPAR-γ and the inhibition of PDE5. Hence NaHS may prove to be beneficial in the treatment of AD.

Indexed as

Amyloid beta-PeptidesAnimalsCaspase 3Cell DeathCyclic Nucleotide Phosphodiesterases, Type 5Enzyme ActivationHippocampusMaleNeuronsNeuroprotective AgentsNeurotoxinsNF-KappaB Inhibitor alphaPeptide FragmentsPhosphorylationPPAR alphaPPAR gammaAmyloid beta-Peptidesamyloid beta-protein (25-35)Caspase 3Cyclic Nucleotide Phosphodiesterases, Type 5Neuroprotective AgentsNeurotoxinsNF-KappaB Inhibitor alphaPeptide FragmentsPPAR alphaPPAR gammasodium bisulfideSulfidesTranscription Factor RelA

Identifiers

PMID27511125
PMCPMC5029968
OpenAlexW2513696185

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.