Evidence map›Paper›PMID 27489506›Full record

ArticleInternational journal of biological sciences2016

Rapamycin Reduced Ischemic Brain Damage in Diabetic Animals Is Associated with Suppressions of mTOR and ERK1/2 Signaling.

Ping Liu, Xiao Yang, Changchun Hei, Yvonne Meli, Jianguo Niu, Tao Sun, P Andy Li

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.3field-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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  10. Hyperglycemia aggravates ischemic brain damageFrontiers in endocrinology · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020
    Review
  16. Article
  17. Article
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  19. Review
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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

7 authors at 2 institutions in 2 countries.

Ping Liu1. Department of Endocrinology, General Hospital of Ningxia Medical University, Yinchuan 750004, China; 2. Department of Pharmaceutical Sciences, Biomanufacturing Research Institute Biotechnology Enterprise (BRITE), North Carolina Central University, 1801 Fayetteville Street, Durham, NC 27707, USA.
Xiao Yang3. Neuroscience Center, General Hospital of Ningcia Medical University, and Key Laboratory of Craniocerebral Diseases of Ningxia Hui Autonomous Region, Yinchuan 750004, China; 2. Department of Pharmaceutical Sciences, Biomanufacturing Research Institute Biotechnology Enterprise (BRITE), North Carolina Central University, 1801 Fayetteville Street, Durham, NC 27707, USA.
Changchun Hei2. Department of Pharmaceutical Sciences, Biomanufacturing Research Institute Biotechnology Enterprise (BRITE), North Carolina Central University, 1801 Fayetteville Street, Durham, NC 27707, USA; 4. Department of Human Anatomy, Histology and Embryology, Ningxia Medical University, Yinchuan 75004, China.
Yvonne Meli2. Department of Pharmaceutical Sciences, Biomanufacturing Research Institute Biotechnology Enterprise (BRITE), North Carolina Central University, 1801 Fayetteville Street, Durham, NC 27707, USA.
Jianguo Niu4. Department of Human Anatomy, Histology and Embryology, Ningxia Medical University, Yinchuan 75004, China.
Tao Sun4. Department of Human Anatomy, Histology and Embryology, Ningxia Medical University, Yinchuan 75004, China.
P Andy Li2. Department of Pharmaceutical Sciences, Biomanufacturing Research Institute Biotechnology Enterprise (BRITE), North Carolina Central University, 1801 Fayetteville Street, Durham, NC 27707, USA.
Ningxia Medical University · CNNorth Carolina Central University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The objectives of the present study are to investigate the activation of mTOR and ERK1/2 signaling after cerebral ischemia in diabetic rats and to examine the neuroprotective effects of rapamycin. Ten minutes transient global cerebral ischemia was induced in straptozotocin-induced diabetic hyperglycemic rats and non-diabetic, euglycemic rats. Brain samples were harvested after 16 h of reperfusion. Rapamycin or vehicle was injected 1 month prior to the induction of ischemia. The results showed that diabetes increased ischemic neuronal cell death and associated with elevations of p-P70S6K and Ras/ERK1/2 and suppression of p-AMPKα. Rapamycin ameliorated diabetes-enhanced ischemic brain damage and suppressed phosphorylation of P70S6K and ERK1/2. It is concluded that diabetes activates mTOR and ERK1/2 signaling pathways in rats subjected to transient cerebral ischemia and inhibition of mTOR by rapamycin reduces ischemic brain damage and suppresses the mTOR and ERK1/2 signaling in diabetic settings.

Indexed as

AMP-Activated Protein KinasesAnimalsBlood GlucoseBlotting, WesternBrain IschemiaCerebral CortexDiabetes Mellitus, ExperimentalDNA FragmentationIn Situ Nick-End LabelingMaleMAP Kinase Signaling SystemRatsRats, WistarSirolimusTOR Serine-Threonine KinasesAMP-Activated Protein KinasesBlood GlucoseSirolimusTOR Serine-Threonine KinasesCerebral ischemiaDiabetesERK1/2mTORRapamycin

Identifiers

PMID27489506
PMCPMC4971741
OpenAlexW2515533414

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.