Evidence map›Paper›PMID 23353638›Full record

ArticleExperimental neurology2013

Intranasal delivery of cell-penetrating anti-NF-κB peptides (Tat-NBD) alleviates infection-sensitized hypoxic-ischemic brain injury.

Dianer Yang, Yu-Yo Sun, Xiaoyi Lin, Jessica M Baumann, R Scott Dunn, Diana M Lindquist, Chia-Yi Kuan

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
9.8field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

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  12. Intranasal Administration ofPharmaceutics · 2022
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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 1 institution in 1 country.

Dianer Yang *Division of Developmental Biology, Department of Pediatrics, Cincinnati's Children's Hospital Medical Center, Cincinnati, OH 45229.
Yu-Yo Sun *Division of Developmental Biology, Department of Pediatrics, Cincinnati's Children's Hospital Medical Center, Cincinnati, OH 45229.
Xiaoyi LinDivision of Developmental Biology, Department of Pediatrics, Cincinnati's Children's Hospital Medical Center, Cincinnati, OH 45229.
Jessica M BaumannDivision of Developmental Biology, Department of Pediatrics, Cincinnati's Children's Hospital Medical Center, Cincinnati, OH 45229.
R Scott DunnImaging Research Center, Department of Radiology, Cincinnati's Children's Hospital Medical Center, Cincinnati, OH 45229.
Diana M LindquistImaging Research Center, Department of Radiology, Cincinnati's Children's Hospital Medical Center, Cincinnati, OH 45229.
Chia-Yi KuanDivision of Developmental Biology, Department of Pediatrics, Cincinnati's Children's Hospital Medical Center, Cincinnati, OH 45229.
Cincinnati Children's Hospital Medical Center · US

Funding

White Matter Protection in Acute Ischemic StrokeR21NS074559 · NINDS · EMORY UNIVERSITY · PI KUAN, CHIA-YI · 2011 to 2012
$421k
NINDS NIH HHS NS074559NINDS NIH HHS R21 NS074559
6 · The paper itself

Abstract

Perinatal infection aggravates neonatal hypoxic-ischemic (HI) brain injury and may interfere with therapeutic hypothermia. While the NF-κB signaling pathway has been implicated in microglia activation in infection-sensitized HI, the current therapeutic strategies rely on systemic intervention, which could impair neonatal immunity and increase the risk of severe infection. To devise a brain-targeted anti-NF-κB strategy, we examined the effects of intranasal delivery of tat-NBD peptides in two animal models of neonatal infection-sensitized HI. Kinetic experiments showed that tat-NBD peptides entered the olfactory bulbs rapidly (10-30 min) and peaked in the cerebral cortex around 60 min after intranasal application in P7 rats. Further, intranasal delivery of 1.4 mg/kg tat-NBD, which is only 7% of the intravenous dose in past studies, markedly attenuated NF-κB signaling, microglia activation, and brain damage triggered by HI with 4 or 72 h pre-exposure to the bacterial endotoxin lipopolysaccharide (LPS). In contrast, intranasal delivery of mutant tat-NBD peptides or systemic application of minocycline failed to block LPS-sensitized HI injury. Yet, intranasal delivery of up to 5.6 mg/kg tat-NBD peptides immediately after pure-HI insult showed little protection, likely due to its rapid clearance from the brain and inability to inhibit parenchymal plasminogen activators. Together, these results suggest a novel therapy of infection-sensitized HI brain injury in newborns.

Indexed as

Administration, IntranasalAnalysis of VarianceAnimalsAnimals, NewbornBrainCalcium-Binding ProteinsCD11b AntigenDisease Models, AnimalElectrophoretic Mobility Shift AssayFemaleHypoxia-Ischemia, BrainIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMagnetic Resonance SpectroscopyMaleMatrix Metalloproteinase 2Aif1 protein, ratCalcium-Binding ProteinsCD11b AntigenIkbkg protein, ratIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMatrix Metalloproteinase 2Matrix Metalloproteinase 9Microfilament ProteinsNF-kappa BPeptidesTetrazolium SaltstriphenyltetrazoliumHypoxia–ischemiaMicrogliaNeuroinflammationNF-kB

Identifiers

PMID23353638
PMCPMC4064308
OpenAlexW1998481986

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.