Evidence map›Paper›PMID 23521913›Full record

ArticleCNS neuroscience & therapeutics2013

Glutathione prevents free fatty acids-induced oxidative stress and apoptosis in human brain vascular endothelial cells through Akt pathway.

Hou-Guang Zhou, Ling Liu, Yu Zhang, Yan-Yan Huang, Ying-Hong Tao, Shuo Zhang, Jing-Jing Su, Yu-Ping Tang, Zhuang-Li Guo, Ren-Ming Hu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 8% 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, 38 citations in OpenAlex.

  1. Trial
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  13. Insulin Resistance and Oxidative Stress in the Brain: What's New?International journal of molecular sciences · 2019
    Review
  14. Article
  15. Article
  16. The Role of Nrf2 in Cardiovascular Function and Disease.Oxidative medicine and cellular longevity · 2017
    Review
  17. Review
  18. Article
  19. Article
  20. ROS signaling and redox biology in endothelial cells.Cellular and molecular life sciences : CMLS · 2015
    Review
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

11 authors at 4 institutions in 1 country.

Hou-Guang ZhouDepartment of Geriatrics Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Ling Liu
Yu Zhang
Yan-Yan Huang
Ying-Hong Tao
Shuo Zhang
Jing-Jing Su
Yu-Ping Tang
Zhuang-Li Guo
Ren-Ming Hu
Qiang Dong
Fudan University · CNNanjing General Hospital of Nanjing Military Command · CNQingdao University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe damage of human brain vascular endothelial cells (HBVECs) is the key pathogenesis of diabetes-associated cerebral vascular complications. The aim of this study was to elucidate the effects of glutathione (GSH) on free fatty acids (FFAs)-induced HBVECs apoptosis, oxidative stress, and the involved possible signaling pathway.

methodsAfter culturing HBVECs for 72 h with GSH and FFAs, we determined cell proliferation by CCK8, detected apoptosis by caspase-3 and Annexin V-FITC/PI staining, and judged oxygen stress by determining the reactive oxygen species (ROS) and the mitochondrial membrane potential (MMP). We investigated whether the Akt pathway was involved in FFAs-induced signaling pathway alteration and whether GSH influenced the above effects.

resultsAfter being cultured in 200 μM FFAs for 72 h, the HBVECs proliferation significantly decreased; HBVECs apoptosis increased; the ROS levels increased; and the HBVECs MMP subsequently decreased. FFAs induced a significant decrease in phosphorylated active Akt. These alterations were obviously prevented when 1 mM GSH was added to culture medium containing FFAs, and the above effects of GSH were blocked by Akt inhibitor.

conclusionGSH may prevent FFAs-induced HBVECs damage, oxidative stress, and apoptosis through activating the Akt pathway.

Indexed as

Oxidative StressApoptosisBrainCells, CulturedCell SurvivalEndothelial CellsFatty Acids, NonesterifiedGlutathioneHumansProto-Oncogene Proteins c-aktSignal TransductionFatty Acids, NonesterifiedGlutathioneProto-Oncogene Proteins c-akt

Identifiers

PMID23521913
PMCPMC6493493
OpenAlexW2128091510

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.