Evidence map›Paper›PMID 31545434›Full record

ArticleInternational journal of molecular medicine2019

Fish oils protects against cecal ligation and puncture‑induced septic acute kidney injury via the regulation of inflammation, oxidative stress and apoptosis.

Zhaoheng Lin, Jing Jin, Xiyun Shan

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  8. Annexin A1 (Ac2-26)-dependent Fpr2 receptor alleviates sepsis-induced acute kidney injury by inhibiting inflammation and apoptosis in vivo and in vitro.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
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  16. Roflumilast, a Phosphodiesterases-4 (PDE4) Inhibitor, Alleviates Sepsis‑induced Acute Kidney Injury.Medical science monitor : international medical journal of experimental and clinical research · 2020
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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.

Zhaoheng LinIntensive Care Unit, The People's Hospital of Xishuangbanna Dai Nationality Autonomous Prefecture, Jinghong, Yunnan 666100, P.R. China.
Jing JinIntensive Care Unit, The People's Hospital of Xishuangbanna Dai Nationality Autonomous Prefecture, Jinghong, Yunnan 666100, P.R. China.
Xiyun ShanIntensive Care Unit, The People's Hospital of Xishuangbanna Dai Nationality Autonomous Prefecture, Jinghong, Yunnan 666100, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Septic acute kidney injury (AKI) is usually caused by sepsis. ω3 fatty acid has been reported to suppress sepsis‑induced organ dysfunction to a certain degree. The present study aimed to investigate the effects of ω3 fatty acid in septic renal injury. Sprague Dawley rats were used to establish a cecal ligation and puncture (CLP) model in order to mimic the development of septic injury. The rats were treated with dexamethasone and fish oils (FOs) for 4 days prior to CLP. Alterations in the morphology of the tissues, the renal function and the induction of inflammation, oxidative stress and apoptosis were evaluated. The effects of FOs on nuclear factor‑κB (NF‑κB), JAK2/STAT3 and p38‑MAPK were determined. The rats of the CLP model group exhibited low survival rates and increased expression of serum creatine, blood urea nitrogen, neutrophil gelatinase‑associated lipocalin, kidney injury molecule‑1 and of proinflammatory cytokines. In addition, the levels of the markers of oxidative injury and apoptosis were increased. The induction of renal injury was notably reversed by administration of dexamethasone and FOs. The expression levels of the protein markers involved in inflammation and apoptosis were measured and the results indicated that FOs inhibited JAK/STAT3 and p‑38MAPK signaling, while they concomitantly increased the expression of NF‑κB. The present study highlighted that FOs improve CLP‑induced mortality and renal injury by inhibiting inflammation, oxidative stress and apoptosis.

Indexed as

Acute Kidney InjuryAnimalsApoptosisBlood Urea NitrogenCecumDisease Models, AnimalFish OilsInflammationJanus KinasesKidneyLigationMaleNF-kappa BOxidative Stressp38 Mitogen-Activated Protein KinasesProtective AgentsFish OilsJanus KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesProtective AgentsSTAT3 Transcription Factor

Identifiers

PMID31545434
PMCPMC6777667
OpenAlexW2972388089

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.