Evidence map›Paper›PMID 38501503›Full record

ArticleImmunity, inflammation and disease2024

Fortunellin ameliorates LPS-induced acute lung injury, inflammation, and collagen deposition by restraining the TLR4/NF-κB/NLRP3 pathway.

Danjuan Liu, Rongjie Guo, Bingbing Shi, Min Chen, Shuoyun Weng, Junting Weng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Danjuan LiuDepartment of Critical Care Medicine, the Affiliated Hospital of Putian University, Putian, China.ORCID 0000-0002-0923-4028
Rongjie GuoDepartment of Critical Care Medicine, the Affiliated Hospital of Putian University, Putian, China.
Bingbing ShiDepartment of Critical Care Medicine, the Affiliated Hospital of Putian University, Putian, China.
Min ChenDepartment of Critical Care Medicine, the Affiliated Hospital of Putian University, Putian, China.
Shuoyun WengSchool of Ophthalmology & Optometry, Wenzhou Medical University, Wenzhou, China.
Junting WengDepartment of Critical Care Medicine, the Affiliated Hospital of Putian University, Putian, China.
Putian University · CNWenzhou Medical University · CN

Funding

Natural Science Foundation of Fujian Province of China 2020J011253Science and Technology Project of Putian City, Fujian Province 2020S3F008
6 · The paper itself

Abstract

objectiveAcute lung injury (ALI) is the prevalent respiratory disease of acute inflammation with high morbidity and mortality. Fortunellin has anti-inflammation property, but its role in ALI remains elusive. Thus, this study clarified the function of fortunellin on ALI pathogenesis.

methodsThe ALI mouse model was established by lipopolysaccharide (LPS) induction, and lung tissue damage was evaluated utilizing hematoxylin-eosin (HE) staining. The edema of lung tissue was measured by the lung wet/dry (W/D) ratio. The lung capillary permeability was reflected by the protein content in bronchoalveolar lavage fluid (BALF). Inflammatory cell infiltration was measured by the evaluation of the content of myeloperoxidase (MPO), neutrophils, and leukocytes in BALF. Cell apoptosis was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The secretions of inflammatory cytokines were quantified using enzyme-linked immunosorbent assay (ELISA) assays. Lung tissue collagen deposition was evaluated by Masson staining.

resultsFortunellin attenuated LPS-induced lung tissue damage and reduced the W/D ratio, the content of MPO in lung tissue, the total protein contents in BALF, and the neutrophils and leukocytes number. Besides, fortunellin alleviated LPS-stimulated lung tissue apoptosis, inflammatory response, and collagen deposition. Furthermore, Fortunellin repressed the activity of the Toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB)/NLR Family Pyrin Domain Containing 3 (NLRP3) pathway in the LPS-stimulated ALI model and LPS-induced RAW264.7 cells. Moreover, fortunellin attenuated LPS-stimulated tissue injury, apoptosis, inflammation, and collagen deposition of the lung via restraining the TLR4/NF-κB/NLRP3 pathway.

conclusionFortunellin attenuated LPS-stimulated ALI through repressing the TLR4/NF-κB/NLRP3 pathway. Fortunellin may be a valuable drug for ALI therapy.

Indexed as

Acute Lung InjuryFlavonoidsGlycosidesNF-kappa BAnimalsCollagenInflammationLipopolysaccharidesMiceNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionToll-Like Receptor 4CollagenFlavonoidsfortunellinGlycosidesLipopolysaccharidesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinToll-Like Receptor 4ALIapoptosiscollagen depositionFortunellininflammatory responseTLR4/NF-κB/NLRP3

Identifiers

PMID38501503
PMCPMC10949398
OpenAlexW4392956432

What OpenQuestion holds

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LicenceCC BY
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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.