Evidence map›Paper›PMID 30711510›Full record

ArticleBrain, behavior, and immunity2019

Rh-IFN-α attenuates neuroinflammation and improves neurological function by inhibiting NF-κB through JAK1-STAT1/TRAF3 pathway in an experimental GMH rat model.

Peng Li, Gang Zhao, Yan Ding, Tianyi Wang, Jerry Flores, Umut Ocak, Pei Wu, Tongyu Zhang, Jun Mo, John H Zhang and 1 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  6. Mechanisms of hydrocephalus after intraventricular haemorrhage: a review.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
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  20. Recombinant CCL17 Enhances Hematoma Resolution and Activation of CCR4/ERK/Nrf2/CD163 Signaling Pathway After Intracerebral Hemorrhage in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Peng LiDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States; Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou 510180, China; Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou 510180, China.
Gang ZhaoDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States; Department of Emergency Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming 650101, China; Traumatic Research Center of Yunnan Province, Kunming 650101, China.
Yan DingDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States.
Tianyi WangDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States.
Jerry FloresDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States.
Umut OcakDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States.
Pei WuDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States.
Tongyu ZhangDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States.
Jun MoDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States.
John H ZhangDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States; Departments of Anesthesiology, Neurosurgery and Neurology, Loma Linda University School of Medicine, Loma Linda, CA 92354, United States.
Jiping TangDepartment of Physiology and Pharmacology, Basic Science, School of Medicine, Loma Linda University, Loma Linda, CA 92354, United States. Electronic address: jtang@llu.edu.
Loma Linda University · USGuangzhou First People's Hospital · CNKunming Medical University · CN

Funding

Investigating the role of mast cells in neonatal germinal matrix hemorrhageR21NS101284 · NINDS · LOMA LINDA UNIVERSITY · PI TANG, JIPING · 2017 to 2018
$435k
NINDS NIH HHS R21 NS101284
6 · The paper itself

Abstract

Neuroinflammation occurs after germinal matrix hemorrhage (GMH) and induces secondary brain injury. Interferon-α (IFN-α) has been shown to exert anti-inflammatory effects in infectious diseases via activating IFNAR and its downstream signaling. We aimed to investigate the anti-inflammatory effects of Recombinant human IFN-α (rh-IFN-α) and the underlying mechanisms in a rat GMH model. Two hundred and eighteen P7 rat pups of both sexes were subjected to GMH by an intraparenchymal injection of bacterial collagenase. Rh-IFN-α was administered intraperitoneally. Small interfering RNA (siRNA) of IFNAR, and siRNA of tumor necrosis factor receptor associated factor 3 (TRAF3) were administered through intracerebroventricular (i.c.v.) injections. JAK1 inhibitor ruxolitinib was given by oral lavage. Post-GMH evaluation included neurobehavioral function, Nissl staining, Western blot analysis, and immunofluorescence. Our results showed that endogenous IFN-α and phosphorylated IFNAR levels were increased after GMH. Administration of rh-IFN-α improved neurological functions, attenuated neuroinflammation, inhibited microglial activation, and ameliorated post-hemorrhagic hydrocephalus after GMH. These observations were concomitant with IFNAR activation, increased expression of phosphorylated JAK1, phosphorylated STAT1 and TRAF3, and decreased levels of phosphorylated NF-κB, IL-6 and TNF-α. Specifically, knockdown of IFNAR, JAK1 and TRAF3 abolished the protective effects of rh-IFN-α. In conclusion, our findings demonstrated that rh-IFN-α treatment attenuated neuroinflammation, neurological deficits and hydrocephalus formation through inhibiting microglial activation after GMH, which might be mediated by IFNAR/JAK1-STAT1/TRAF3/NF-κB signaling pathway. Rh-IFN-α may be a promising therapeutic agent to attenuate brain injury via its anti-inflammatory effect.

Indexed as

AnimalsAnimals, NewbornBrain InjuriesCerebral Intraventricular HemorrhageCytokinesDisease Models, AnimalFemaleHumansI-kappa B ProteinsInflammationInterferon-alphaJanus Kinase 1MaleMicrogliaNeuroimmunomodulationNF-kappa BCytokinesI-kappa B ProteinsInterferon-alphaJanus Kinase 1NF-kappa BStat1 protein, ratSTAT1 Transcription FactorTNF Receptor-Associated Factor 3Germinal matrix hemorrhageHydrocephalusInflammationInterferon-αMicroglia

Identifiers

PMID30711510
PMCPMC6591046
OpenAlexW2912531099

What OpenQuestion holds

Textmetadata
LicenceTDM
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.