Evidence map›Paper›PMID 25170301›Full record

ArticleInternational journal of biological sciences2014

Intermittent hypothermia is neuroprotective in an in vitro model of ischemic stroke.

Sui-yi Xu, Ya-fang Hu, Wei-pin Li, Yong-ming Wu, Zhong Ji, Sheng-nan Wang, Ke Li, Su-yue Pan

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Sui-yi Xu1. Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; ; 2. Department of Neurosurgery, Shenzhen Key Laboratory of Neurosurgery, Shenzhen Second People's Hospital, Shenzhen University 1st Affiliated Hospital, Shenzhen 518035, China;
Ya-fang Hu1. Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China;
Wei-pin Li2. Department of Neurosurgery, Shenzhen Key Laboratory of Neurosurgery, Shenzhen Second People's Hospital, Shenzhen University 1st Affiliated Hospital, Shenzhen 518035, China;
Yong-ming Wu1. Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China;
Zhong Ji1. Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China;
Sheng-nan Wang1. Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China;
Ke Li3. Research Center of Clinical Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Su-yue Pan1. Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China;
Nanfang Hospital · CNShenzhen Second People's Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate whether the intermittent hypothermia (IH) protects neurons against ischemic insult and the potential molecular targets using an in vitro ischemic model of oxygen glucose deprivation (OGD).

methodsFetal rat cortical neurons isolated from Day E18 rat embryos were subjected to 90-min OGD and hypothermia treatments during reoxygenation before examining the changes in microscopic morphology, cell viability, microtubule- associated protein 2 (MAP-2) release, intracellular pH value and calcium, reactive oxygen species (ROS) generation, mitochondrial membrane potential (△Ψm) and neuronal death using cell counting kit (CCK-8), enzyme-linked immunosorbent assay (ELISA), BCECF AM, Fluo-3 AM, DCFH-DA and dihydroethidium (DHE), JC-1 staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), respectively.

results90-min OGD induced morphologic abnormalities, cell viability decline, MAP-2 release, intracellular acidosis, calcium overload, increased ROS generation, △Ψm decrease and cell death in primary neurons, which was partially inhibited by continuous hypothermia (CH) and intermittent hypothermia (IH). Interestingly, 6-h CH was insufficient to reduce intracellular calcium overload and stabilize mitochondrial membrane potential (△Ψm), while 12-h CH was effective in reversing the above changes. All IH treatments (6×1 h, 4×1.5 h or 3×2 h) effectively attenuated intracellular free calcium overload, inhibited ROS production, stabilized mitochondrial membrane potential (△Ψm) and reduced delayed cell death in OGD-treated cells. However, only IH intervals longer than 1.5 h appeared to be effective in preventing cell viability loss and intracellular pH decline.

conclusionBoth CH and IH were neuroprotective in an in vitro model of ischemic stroke, and in spite of shorter hypothermia duration, IH could provide a comparable neuroprotection to CH.

Indexed as

AnimalsCells, CulturedCell SurvivalEmbryo, MammalianFemaleHypothermiaIn Situ Nick-End LabelingNeuronsPregnancyRatsReactive Oxygen SpeciesStrokeReactive Oxygen SpeciesHypothermiaIschemic strokeNeuroprotectionPrimary neuronal culture.

Identifiers

PMID25170301
PMCPMC4147221
OpenAlexW2147548066

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.