Evidence map›Paper›PMID 16367929›Full record

ArticleClinical and experimental immunology2006

Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model.

B H M Heijnen, I H Straatsburg, N D Padilla, G J Van Mierlo, C E Hack, T M Van Gulik

Registry-linked trialOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03791476 (A Phase I/II,Single Center,Randomized,Double-Blind,Placebo-Controlled Study to Evaluate the Feasibility of Using Human Recombinant C1 Inhibitor), which is not on this map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% 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.

NCT03791476 phase1unknown statusnot on this mapstarted 2019, after this paper: background citation

A Phase I/II,Single Center,Randomized,Double-Blind,Placebo-Controlled Study to Evaluate the Feasibility of Using Human Recombinant C1 Inhibitor(RUCONEST®) as a Therapeutic Strategy to Reduce the Incidence of Delayed Graft Function in Recipients of Kidneys From Donation After Cardio-Circulatory Death

TypeinterventionalSponsorUniversity of Wisconsin, MadisonRan2019 to 2022Enrolled20ConditionsKidney FailureArmsrhC1INH, Saline Solution
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 61 citations in OpenAlex.

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  18. Hyperbaric oxygen therapy reduces the severity of ischaemia, preservation and reperfusion injury in a rat model of liver transplantation.HPB : the official journal of the International Hepato Pancreato Biliary Association · 2012
    Article
  19. Innate immune cells in liver inflammation.Mediators of inflammation · 2012
    Review
  20. Review
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

6 authors at 1 institution in 1 country.

B H M HeijnenDepartment of Surgery, Surgical Laboratory, Academic Medical Centre, Amsterdam, The Netherlands.
I H Straatsburg
N D Padilla
G J Van Mierlo
C E Hack
T M Van Gulik
Sanquin · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the complement system contributes to the pathogenesis of ischaemia/reperfusion (I/R) injury. We evaluated inhibition of the classical pathway of complement using C1-inhibitor (C1-inh) in a model of 70% partial liver I/R injury in male Wistar rats (n = 35). C1-inh was administered at 100, 200 or 400 IU/kg bodyweight, 5 min before 60 min ischaemia (pre-I) or 5 min before 24 h reperfusion (end-I). One hundred IU/kg bodyweight significantly reduced the increase of plasma levels of activated C4 as compared to albumin-treated control rats and attenuated the increase of alanine aminotransferase (ALT). These effects were not better with higher doses of C1-inh. Administration of C1-inh pre-I resulted in lower ALT levels and higher bile secretion after 24 h of reperfusion than administration at end-I. Immunohistochemical assessment indicated that activated C3, the membrane attack complex C5b9 and C-reactive protein (CRP) colocalized in hepatocytes within midzonal areas, suggesting CRP is a mediator of I/R-induced, classical complement activation in rats. Pre-ischaemic administration of C1-inh is an effective pharmacological intervention to protect against liver I/R injury.

Indexed as

Alanine TransaminaseAnimalsBileBiomarkersComplement C1 Inhibitor ProteinComplement C3aComplement C4aComplement Membrane Attack ComplexComplement Pathway, ClassicalComplement System ProteinsC-Reactive ProteinDrug Administration ScheduleEnzyme-Linked Immunosorbent AssayGlycoproteinsHistocytochemistryIschemiaAlanine TransaminaseBiomarkersComplement C1 Inhibitor ProteinComplement C3aComplement C4aComplement Membrane Attack ComplexComplement System ProteinsC-Reactive ProteinGlycoproteinsSC5b-9 protein complex

Identifiers

PMID16367929
PMCPMC1809558
OpenAlexW2106085405

What OpenQuestion holds

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Registered trials

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.