Evidence map›Paper›PMID 24952361›Full record

ArticleNeurobiology of disease2014

Systemic hemin therapy attenuates blood-brain barrier disruption after intracerebral hemorrhage.

Xiangping Lu, Jing Chen-Roetling, Raymond F Regan

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-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

30 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Heme: The Lord of the Iron Ring.Antioxidants (Basel, Switzerland) · 2023
    Review
  4. Review
  5. Article
  6. Endogenous zinc protoporphyrin formation critically contributes to hemorrhagic stroke-induced brain damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  7. Potential therapeutic effects of Nrf2 activators on intracranial hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Review
  8. Review
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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

3 authors at 1 institution in 1 country.

Xiangping LuDepartment of Emergency Medicine, Thomas Jefferson University, 1025 Walnut Street, College Building Room 813, Philadelphia, PA 19107, United States.
Jing Chen-RoetlingDepartment of Emergency Medicine, Thomas Jefferson University, 1025 Walnut Street, College Building Room 813, Philadelphia, PA 19107, United States.
Raymond F ReganDepartment of Emergency Medicine, Thomas Jefferson University, 1025 Walnut Street, College Building Room 813, Philadelphia, PA 19107, United States. Electronic address: Raymond.Regan@jefferson.edu.
Thomas Jefferson University · US

Funding

Protective Effect of Hemin Preconditioning after Intracerebral HemorrhageR01NS079500 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI REGAN, RAYMOND F · 2012 to 2015
$1.3M
NINDS NIH HHS NS079500NINDS NIH HHS R01 NS079500
6 · The paper itself

Abstract

Injury to the blood-brain barrier (BBB) is a key feature of intracerebral hemorrhage (ICH) and may contribute to perihematomal cell injury. Pretreatment with the heme oxygenase (HO)-1 inducer hemin improves barrier function and neurological outcome in experimental models of traumatic and ischemic CNS injury. Since hemin is already in clinical use to treat acute porphyrias, this translational study was designed to test its effect on BBB function when initiated after ICH in two mouse models. At a dose similar to those used in most preconditioning studies (26mg/kg i.p.), post-hemorrhage treatment with hemin reduced parenchymal extravasation of Evans blue by about three-quarters in both the blood injection and collagenase ICH models. Similar efficacy was observed when treatment was begun at 1 or 3h. At the lower dose that is currently in clinical use (4mg/kg beginning at 3h), hemin also improved barrier function in both models, as assessed by both Evans blue and FITC-dextran leakage; however, it was somewhat less potent, reducing Evans blue leakage by about half. This dose was nevertheless sufficient to attenuate striatal cell loss and accelerate neurological recovery. Consistent with prior observations, striatal HO-1 expression was increased by hemin, and was localized to perivascular cells. These results suggest that hemin may be an effective therapy for ICH with a clinically relevant time window. Further study of the repurposing of this old drug seems warranted.

Indexed as

AnimalsBlood-Brain BarrierBrain EdemaCapillary PermeabilityCell SurvivalCerebral HemorrhageCorpus StriatumDisease Models, AnimalFemaleHeme Oxygenase-1HeminMaleMembrane ProteinsMiceNeuroprotective AgentsTime FactorsHeme Oxygenase-1HeminHmox1 protein, mouseMembrane ProteinsNeuroprotective AgentsHemeHeme oxygenasePreconditioningStroke

Identifiers

PMID24952361
PMCPMC4221186
OpenAlexW2069070912

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.