Evidence map›Paper›PMID 40728674›Full record

ArticleInflammopharmacology2025

Sunitinib treatment reduces proinflammatory cytokine levels and mortality rates by suppressing the NLRP3 inflammasome signaling pathway in sepsis.

Ahmet Kucuk, Nurhak Aksungur, Zekai Halici, Taha Tavaci, Mustafa Ozkaraca, Behzat Tebrizi

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Article in Inflammopharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. 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.

Ahmet KucukDepartment of General Surgery, Faculty of Medicine, Atatürk University, Erzurum, Turkey. ahmetkucuk0594@gmail.com.ORCID http://orcid.org/0009-0002-6421-6436
Nurhak AksungurDepartment of General Surgery, Faculty of Medicine, Atatürk University, Erzurum, Turkey.ORCID http://orcid.org/0000-0003-4477-5775
Zekai HaliciDepartment of Clinical Pharmacology, Faculty of Medicine, Atatürk University, Erzurum, Turkey.ORCID http://orcid.org/0000-0001-6854-6059
Taha TavaciDepartment of Clinical Pharmacology, Faculty of Medicine, Sakarya University, Sakarya, Turkey.ORCID http://orcid.org/0000-0002-8284-8317
Mustafa OzkaracaDepartment of Pathology, Faculty of Veterian, Cumhuriyet University, Sivas, Turkey.ORCID http://orcid.org/0000-0001-9765-4569
Behzat TebriziDepartment of Pathology, Faculty of Veterian, Dicle University, Diyarbakir, Turkey.ORCID http://orcid.org/0000-0002-9075-7239

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGiven the elevated mortality rates and significant treatment costs associated with sepsis, characterized by a dysregulated host response to infection and life-threatening organ dysfunction, the search for treatment strategies involving new and potentially effective agents is essential. Sunitinib, a tyrosine kinase inhibitor, shows promise for mitigating increased inflammation in sepsis through its modulation of specific molecular pathways. This study investigates the effects of sunitinib in the treatment of sepsis.

methodsSepsis was induced in rats using the cecal ligation and puncture (CLP) model and sunitinib treatment was administered orally at various dosages. The effects of sunitinib treatment were evaluated through molecular and histopathological methods. The impact of sunitinib treatment on survival was analyzed using Kaplan-Meier survival analysis.

resultsWith low-dose treatment, sunitinib was observed to reduce the levels of proinflammatory cytokines, including interleukin-6, interleukin-8, and TNF-α. However, no reduction was observed with high-dose sunitinib in comparison to the sepsis group. Polymerase chain reaction results indicated that the NLRP3 inflammasome pathway was attenuated with low-dose sunitinib treatment. Furthermore, the extent of sepsis associated histopathological and immunohistochemical changes was reduced with sunitinib treatment, as demonstrated by hematoxylin and eosin staining and immunohistochemical analysis. Survival analysis revealed that the group receiving low-dose sunitinib had the highest survival rate.

conclusionDifferent sunitinib doses in sepsis treatment yield significantly different molecular results, histopathological outcomes, and survival rates. A comprehensive investigation of tyrosine kinase inhibitor drugs such as sunitinib in the treatment of sepsis will enhance the efficacy of sepsis therapies.

Indexed as

CytokinesIndolesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinPyrrolesSepsisSignal TransductionSunitinibAnimalsDisease Models, AnimalDose-Response Relationship, DrugInflammationInflammation MediatorsMaleRatsRats, Sprague-DawleyCytokinesIndolesInflammasomesInflammation MediatorsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratPyrrolesSunitinibCytokineInflammasomeNLRP3SepsisSunitinibSurvival

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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.