Evidence map›Paper›PMID 27718095›Full record

ArticleInflammation2017

Indirubin Inhibits LPS-Induced Inflammation via TLR4 Abrogation Mediated by the NF-kB and MAPK Signaling Pathways.

Jin-Lun Lai, Yu-Hui Liu, Chang Liu, Ming-Pu Qi, Rui-Ning Liu, Xi-Fang Zhu, Qiu-Ge Zhou, Ying-Yu Chen, Ai-Zhen Guo, Chang-Min Hu

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 232 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
232citing papers in PubMed, 2 pooled it
10.9field-weighted citation impact, top 1% 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

232 citing papers in PubMed, 2 syntheses or guidelines pooled it, 465 citations in OpenAlex.

  1. Pooled it
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172 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

Jin-Lun LaiThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Yu-Hui LiuThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Chang LiuThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Ming-Pu QiThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Rui-Ning LiuThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Xi-Fang ZhuThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Qiu-Ge ZhouThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Ying-Yu ChenThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China.
Ai-Zhen GuoThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. aizhen@mail.hzau.edu.cn.
Chang-Min HuThe Faculty of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, China. hcm@mail.hzau.edu.cn.
Huazhong Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Indirubin plays an important role in the treatment of many chronic diseases and exhibits strong anti-inflammatory activity. However, the molecular mode of action during mastitis prophylaxis remains poorly understood. In this study, a lipopolysaccharide (LPS)-induced mastitis mouse model showed that indirubin attenuated histopathological changes in the mammary gland, local tissue necrosis, and neutrophil infiltration. Moreover, indirubin significantly downregulated the production of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). We explored the mechanism whereby indirubin exerts protective effects against LPS-induced inflammation of mouse mammary epithelial cells (MMECs). The addition of different concentrations of indirubin before exposure of cells to LPS for 1 h significantly attenuated inflammation and reduced the concentrations of the three inflammatory cytokines in a dose-dependent manner. Indirubin downregulated LPS-induced cyclooxygenase-2 (COX-2) and Toll-like receptor 4 (TLR4) expression, inhibited phosphorylation of the LPS-induced nuclear transcription factor-kappa B (NF-kB) P65 protein and its inhibitor IkBα of the NF-kB signaling pathway. Furthermore, indirubin suppressed phosphorylation of P38, extracellular signal-regulated kinase (ERK), and c-Jun NH

Indexed as

AnimalsCytokinesDose-Response Relationship, DrugFemaleIndolesInflammationInflammation MediatorsLipopolysaccharidesMAP Kinase Signaling SystemMastitisMiceNF-kappa BSignal TransductionToll-Like Receptor 4CytokinesindirubinIndolesInflammation MediatorsLipopolysaccharidesNF-kappa BTlr4 protein, mouseToll-Like Receptor 4indirubininflammationlipopolysaccharide (LPS)MAPKNF-kBTLR4

Identifiers

PMID27718095
OpenAlexW2528491208

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.