Evidence map›Paper›PMID 38753858›Full record

ArticlePloS one2024

Echinatin attenuates acute lung injury and inflammatory responses via TAK1-MAPK/NF-κB and Keap1-Nrf2-HO-1 signaling pathways in macrophages.

Liuling Luo, Huan Wang, Jinrui Xiong, Xiaorui Chen, Xiaofei Shen, Hai Zhang

Abstract read
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Echinatin inhibits osteoarthritis through the NF-κB signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Article
  5. The role of SIRT1 in kidney diseases.International urology and nephrology · 2025
    Review
  6. 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.

Liuling LuoState Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy/School of Modern Chinese Medicine Industry, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Huan WangState Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy/School of Modern Chinese Medicine Industry, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Jinrui XiongState Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy/School of Modern Chinese Medicine Industry, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Xiaorui ChenState Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy/School of Modern Chinese Medicine Industry, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Xiaofei ShenHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Hai ZhangState Key Laboratory of Southwestern Chinese Medicine Resources, School of Pharmacy/School of Modern Chinese Medicine Industry, Chengdu University of Traditional Chinese Medicine, Chengdu, China.ORCID 0000-0001-6775-1050

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Echinatin is an active ingredient in licorice, a traditional Chinese medicine used in the treatment of inflammatory disorders. However, the protective effect and underlying mechanism of echinatin against acute lung injury (ALI) is still unclear. Herein, we aimed to explore echinatin-mediated anti-inflammatory effects on lipopolysaccharide (LPS)-stimulated ALI and its molecular mechanisms in macrophages. In vitro, echinatin markedly decreased the levels of nitric oxide (NO) and prostaglandin E2 (PGE2) in LPS-stimulated murine MH-S alveolar macrophages and RAW264.7 macrophages by suppressing inducible nitric oxide synthase and cyclooxygenase-2 (COX-2) expression. Furthermore, echinatin reduced LPS-induced mRNA expression and release of interleukin-1β (IL-1β) and IL-6 in RAW264.7 cells. Western blotting and CETSA showed that echinatin repressed LPS-induced activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways through targeting transforming growth factor-beta-activated kinase 1 (TAK1). Furthermore, echinatin directly interacted with Kelch-like ECH-associated protein 1 (Keap1) and activated the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway to enhance heme oxygenase-1 (HO-1) expression. In vivo, echinatin ameliorated LPS-induced lung inflammatory injury, and reduced production of IL-1β and IL-6. These findings demonstrated that echinatin exerted anti-inflammatory effects in vitro and in vivo, via blocking the TAK1-MAPK/NF-κB pathway and activating the Keap1-Nrf2-HO-1 pathway.

Indexed as

Acute Lung InjuryLipopolysaccharidesMAP Kinase Kinase KinasesSignal TransductionAnimalsAnti-Inflammatory AgentsHeme Oxygenase-1InflammationKelch-Like ECH-Associated Protein 1MacrophagesMaleMAP Kinase Kinase Kinase 7Membrane ProteinsMiceNF-E2-Related Factor 2NF-kappa BAnti-Inflammatory AgentsHeme Oxygenase-1Hmox1 protein, mouseKeap1 protein, mouseKelch-Like ECH-Associated Protein 1LipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMembrane ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2NF-kappa B

Identifiers

PMID38753858
PMCPMC11098428

What OpenQuestion holds

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Registered trials

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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.