Evidence map›Paper›PMID 24747165›Full record

ArticleActa pharmacologica Sinica2014

Hydrogen sulfide inhibits homocysteine-induced endoplasmic reticulum stress and neuronal apoptosis in rat hippocampus via upregulation of the BDNF-TrkB pathway.

Hai-Jun Wei, Jin-Hua Xu, Man-Hong Li, Ji-Ping Tang, Wei Zou, Ping Zhang, Li Wang, Chun-Yan Wang, Xiao-Qing Tang

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  13. Article
  14. Hydrogen Sulfide (HCurrent neuropharmacology · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. SIRT1 Mediates HNeurochemical research · 2021
    Article
  19. Review
  20. Review

2 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Hai-Jun WeiInstitute of Neuroscience, Medical College, University of South China, Hengyang 421001, China.
Jin-Hua XuLaboratory Center of Biochemistry and Molecular Biology, University of South China, Hengyang 421001, China.
Man-Hong Li1] Institute of Neuroscience, Medical College, University of South China, Hengyang 421001, China [2] Department of Neurology, Nanhua Affiliated Hospital, University of South China, Hengyang 421001, China.
Ji-Ping Tang1] Institute of Neuroscience, Medical College, University of South China, Hengyang 421001, China [2] Department of Neurology, Nanhua Affiliated Hospital, University of South China, Hengyang 421001, China.
Wei ZouDepartment of Neurology, Nanhua Affiliated Hospital, University of South China, Hengyang 421001, China.
Ping ZhangDepartment of Neurology, Nanhua Affiliated Hospital, University of South China, Hengyang 421001, China.
Li WangDepartment of Anthropotomy, Medical College, University of South China, Hengyang 421001, China.
Chun-Yan WangDepartment of Pathophysiology, Medical College, University of South China, Hengyang 421001, China.
Xiao-Qing TangInstitute of Neuroscience, Medical College, University of South China, Hengyang 421001, China.
University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimHomocysteine (Hcy) can elicit neuronal cell death, and hyperhomocysteinemia is a strong independent risk factor for Alzheimer's disease. The aim of this study was to examine the effects of hydrogen sulfide (H2S) on Hcy-induced endoplasmic reticulum (ER) stress and neuronal apoptosis in rat hippocampus.

methodsAdult male SD rats were intracerebroventricularly (icv) injected with Hcy (0.6 μmol/d) for 7 d. Before Hcy injection, the rats were treated with NaHS (30 or 100 μmol·kg(-1)·d(-1), ip) and/or k252a (1 μg/d, icv) for 2 d. The apoptotic neurons were detected in hippocampal coronal slices with TUNEL staining. The expression of glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), cleaved caspase-12, and BDNF in the hippocampus were examined using Western blotting assays. The generation of H2S in the hippocampus was measured with the NNDPD method.

resultsHcy markedly inhibited the production of endogenous H2S and increased apoptotic neurons in the hippocampus. Furthermore, Hcy induced ER stress responses in the hippocampus, as indicated by the upregulation of GRP78, CHOP, and cleaved caspase-12. Treatment with the H2S donor NaHS increased the endogenous H2S production and BDNF expression in a dose-dependent manner, and significantly reduced Hcy-induced neuronal apoptosis and ER stress responses in the hippocampus. Treatment with k252a, a specific inhibitor of TrkB (the receptor of BDNF), abolished the protective effects of NaHS against Hcy-induced ER stress in the hippocampus.

conclusionH2S attenuates ER stress and neuronal apoptosis in the hippocampus of Hcy-treated rats via upregulating the BDNF-TrkB pathway.

Indexed as

AnimalsApoptosisBrain-Derived Neurotrophic FactorCell LineEndoplasmic Reticulum StressHippocampusHomocysteineHydrogen SulfideHyperhomocysteinemiaMaleNeuronsNeuroprotective AgentsRatsRats, Sprague-DawleyReceptor, trkBSignal TransductionBrain-Derived Neurotrophic FactorHomocysteineHydrogen SulfideNeuroprotective AgentsReceptor, trkB

Identifiers

PMID24747165
PMCPMC4086382
OpenAlexW1974980148

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.