Evidence map›Paper›PMID 28497278›Full record

ArticleInflammation2017

IL-35 Pretreatment Alleviates Lipopolysaccharide-Induced Acute Kidney Injury in Mice by Inhibiting NF-κB Activation.

Linkun Hu, Cheng Chen, Jun Zhang, Kerong Wu, Xuefeng Zhang, Haiyan Liu, Jianquan Hou

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  13. Porous Se@SiOInternational journal of nanomedicine · 2019
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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

7 authors at 4 institutions in 2 countries.

Linkun HuDepartment of Urology, The First Affiliated Hospital of Soochow University, 188 Shizi Rd, Suzhou, 215006, People's Republic of China.
Cheng ChenDepartment of Urology, The First Affiliated Hospital of Soochow University, 188 Shizi Rd, Suzhou, 215006, People's Republic of China.
Jun ZhangDepartment of Urology, The First Affiliated Hospital of Soochow University, 188 Shizi Rd, Suzhou, 215006, People's Republic of China.
Kerong WuCenter of Uro-nephrological Disease, Ningbo First Hospital, NO. 59 Liuting Avenue, Haishu District, Ningbo, 315000, People's Republic of China.
Xuefeng ZhangDepartment of Urology, The First Affiliated Hospital of Soochow University, 188 Shizi Rd, Suzhou, 215006, People's Republic of China.
Haiyan LiuImmunology Programme, Life Sciences Institute and Department of Microbiology and Immunology, National University of Singapore, Singapore, 117456, Singapore. micliuh@nus.edu.sg.
Jianquan HouDepartment of Urology, The First Affiliated Hospital of Soochow University, 188 Shizi Rd, Suzhou, 215006, People's Republic of China. xf192@163.com.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CNNational University of Singapore · SGNingbo First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Septic acute kidney injury (AKI) is a public health problem with high mortality. Suppression of over-active inflammation is considered as a promising strategy for septic AKI. In this study, we evaluated the prophylactic effect of interleukin (IL)-35, the unique immune-suppressive member of IL-12 cytokine family, on lipopolysaccharide (LPS)-induced AKI in mice, and found that compared with control mice given empty vector, mice pretreated with plasmid encoding IL-35 (pIL-35) significantly improved renal function indicated by reduced blood urea nitrogen (BUN) and serum creatinine (SCr), and obviously alleviated renal pathological changes. To explore the underlying protective mechanisms, we found that pIL-35 treatment could robustly reduce the production of renal pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), with no significant impact on IL-10, an anti-inflammatory cytokine. Furthermore, our results revealed that IL-35 pretreatment could potentially inhibit the activation of renal NF-κB signaling pathway in LPS-induced AKI mice. Taken together, our study indicated that IL-35 pretreatment could efficiently prevent LPS-induced AKI via inhibiting NF-κB activation and reducing pro-inflammatory cytokine production, and it might represent a novel therapeutic strategy against septic AKI and other inflammatory renal diseases.

Indexed as

Acute Kidney InjuryAnimalsCytokinesInflammationInterleukinsKidneyLipopolysaccharidesMiceNF-kappa BCytokinesinterleukin-35, mouseInterleukinsLipopolysaccharidesNF-kappa Bacute kidney injuryIL-35NF-κBpreventionsepsis

Identifiers

PMID28497278
OpenAlexW2612881075

What OpenQuestion holds

Textmetadata
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.