Evidence map›Paper›PMID 28025500›Full record

ArticleInternational journal of molecular sciences2016

Glucocorticoids Protect Neonatal Rat Brain in Model of Hypoxic-Ischemic Encephalopathy (HIE).

Benjamin Harding, Katherine Conception, Yong Li, Lubo Zhang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
10.5field-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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 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

4 authors at 2 institutions in 1 country.

Benjamin HardingDivision of Neonatology, Department of Pediatrics, Loma Linda University Children's Hospital, Loma Linda, CA 92354, USA. bharding@llu.edu.
Katherine ConceptionCenter for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA. kconcepcion@llu.edu.
Yong LiCenter for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA. yoli@llu.edu.
Lubo ZhangCenter for Perinatal Biology, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA. lzhang@llu.edu.
Loma Linda University · USLoma Linda University Children's Hospital · US

Funding

Developmental Programming of Ischemic-Sensitive Phenotype in the HeartR01HL118861 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2014 to 2017
$1.8M
NHLBI NIH HHS R01 HL118861
6 · The paper itself

Abstract

Hypoxic-ischemic encephalopathy (HIE) resulting from asphyxia in the peripartum period is the most common cause of neonatal brain damage and can result in significant neurologic sequelae, including cerebral palsy. Currently therapeutic hypothermia is the only accepted treatment in addition to supportive care for infants with HIE, however, many additional neuroprotective therapies have been investigated. Of these, glucocorticoids have previously been shown to have neuroprotective effects. HIE is also frequently compounded by infectious inflammatory processes (sepsis) and as such, the infants may be more amenable to treatment with an anti-inflammatory agent. Thus, the present study investigated dexamethasone and hydrocortisone treatment given after hypoxic-ischemic (HI) insult in neonatal rats via intracerebroventricular (ICV) injection and intranasal administration. In addition, we examined the effects of hydrocortisone treatment in HIE after lipopolysaccharide (LPS) sensitization in a model of HIE and sepsis. We found that dexamethasone significantly reduced rat brain infarction size when given after HI treatment via ICV injection; however it did not demonstrate any neuroprotective effects when given intranasally. Hydrocortisone after HI insult also significantly reduced brain infarction size when given via ICV injection; and the intranasal administration showed to be protective of brain injury in male rats at a dose of 300 µg. LPS sensitization did significantly increase the brain infarction size compared to controls, and hydrocortisone treatment after LPS sensitization showed a significant decrease in brain infarction size when given via ICV injection, as well as intranasal administration in both genders at a dose of 300 µg. To conclude, these results show that glucocorticoids have significant neuroprotective effects when given after HI injury and that these effects may be even more pronounced when given in circumstances of additional inflammatory injury, such as neonatal sepsis.

Indexed as

Administration, IntranasalAnimalsDexamethasoneGlucocorticoidsHydrocortisoneHypoxia-Ischemia, BrainInjections, IntraventricularNeuroprotective AgentsRatsRats, Sprague-DawleyDexamethasoneGlucocorticoidsHydrocortisoneNeuroprotective Agentsdexamethasoneencephalopathyhydrocortisonehypoxic-ischemicintranasallipopolysaccharidesneonatalneuroprotectionRice-Vannucci

Identifiers

PMID28025500
PMCPMC5297652
OpenAlexW2564209709

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.