Evidence map›Paper›PMID 26366999›Full record

ArticlePloS one2015

IL-10 Protects Neurites in Oxygen-Glucose-Deprived Cortical Neurons through the PI3K/Akt Pathway.

Longzai Lin, Hongbin Chen, Yixian Zhang, Wei Lin, Yong Liu, Tin Li, Yongping Zeng, Jianhao Chen, Houwei Du, Ronghua Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Electroacupuncture combined with rTMS promotes neuronal regenerationEuropean journal of histochemistry : EJH · 2026
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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

12 authors at 1 institution in 1 country.

Longzai LinDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Hongbin ChenDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Yixian ZhangInstitute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China; Department of Rehabilitation, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Wei LinDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Yong LiuDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Tin LiDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Yongping ZengDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Jianhao ChenDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Houwei DuDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Ronghua ChenDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Yi TanInstitute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China.
Nan LiuDepartment of Neurology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China; Institute of Cerebral Vascular Disease of Fujian Province, Fuzhou, Fujian, People's Republic of China; Department of Rehabilitation, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Fujian Institute of Microbiology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-10, as a cytokine, has an anti-inflammatory cascade following various injuries, but it remains blurred whether IL-10 protects neurites of cortical neurons after oxygen-glucose deprivation injury. Here, we reported that IL-10, in a concentration-dependent manner, reduced neuronal apoptosis and increased neuronal survival in oxygen-glucose-deprived primary cortical neurons, producing an optimal protective effect at 20ng/ml. After staining NF-H and GAP-43, we found that IL-10 significantly protected neurites in terms of axon length and dendrite number by confocal microscopy. Furthermore, it induced the phosphorylation of AKT, suppressed the activation of caspase-3, and up-regulated the protein expression of GAP-43. In contrast, LY294002, a specific inhibitor of PI3K/AKT, reduced the level of AKT phosphorylation and GAP-43 expression, increased active caspase-3 expression and thus significantly weakened IL-10-mediated protective effect in the OGD-induced injury model. IL-10NA, the IL-10 neutralizing antibody, reduced the level of p-PI3K phosphorylation and increased the expression of active caspase-3. These findings suggest that IL-10 provides neuroprotective effects by protecting neurites through PI3K/AKT signaling pathway in oxygen-glucose-deprived primary cortical neurons.

Indexed as

AnimalsCaspase 3Cell HypoxiaCells, CulturedCerebral CortexGAP-43 ProteinGlucoseInterleukin-10NeuritesNeuroprotective AgentsOxidative StressOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyCaspase 3GAP-43 ProteinGlucoseInterleukin-10Neuroprotective AgentsOxygenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID26366999
PMCPMC4569574
OpenAlexW1884483916

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.