Evidence map›Paper›PMID 34986734›Full record

ArticleBioengineered2022

Ramelteon protects against human pulmonary microvascular endothelial cell injury induced by lipopolysaccharide (LPS) via activating nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway.

Wenjun Yang, Yang Zhang, Dahao Lu, Tianfeng Huang, Keshi Yan, Weiwei Wang, Ju Gao

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
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  7. Article
  8. Preventive effects of Ramelteon on bleomycin-induced pulmonary fibrosis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Article
  9. The Extracts Derived fromMolecules (Basel, Switzerland) · 2024
    Article
  10. Article
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  12. Review
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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 1 institution in 1 country.

Wenjun YangDepartment of Anesthesiology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou City, Jiangsu Province, China.
Yang ZhangDepartment of Anesthesiology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou City, Jiangsu Province, China.
Dahao LuDepartment of Anesthesiology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou City, Jiangsu Province, China.
Tianfeng HuangDepartment of Anesthesiology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou City, Jiangsu Province, China.
Keshi YanDepartment of Anesthesiology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou City, Jiangsu Province, China.
Weiwei WangDepartment of Anesthesiology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou City, Jiangsu Province, China.
Ju GaoDepartment of Anesthesiology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou City, Jiangsu Province, China.
Northern Jiangsu People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is classified as a moderate or mild acute respiratory distress syndrome and is a prominent cause of morbidity and mortality among the critically ill population. Ramelteon is a melatonin receptor agonist with anti-inflammatory and antioxidant effects. The current study investigated the role of ramelteon in lipopolysaccharide (LPS)-induced human pulmonary microvascular endothelial cells (HPMECs) and its potential regulatory mechanisms. A CCK-8 assay was used to examine the effect of ramelteon on the viability of LPS-induced HPMECs, HPMECs treated with ML385 [a Nrf2 inhibitor] and HPMECs treated with SnPP [a HO-1 inhibitor]. The Nrf2/HO-1 signaling pathway was additionally assessed by performing Western blotting. The levels of oxidative stress and inflammatory cytokines in HPMECs were detected using kits and reverse transcription-quantitative PCR. Cell apoptosis was evaluated via TUNEL staining. Furthermore, cell permeability was assessed using a FITC-dextran fluorescent probe, ZO-1 and occludin expression was determined via Western blotting. The results demonstrated that ramelteon elevated HPMEC viability after LPS stimulation. Additionally, ramelteon markedly reduced LPS-induced oxidative stress, inflammation and apoptosis. Moreover, cell permeability was notably decreased in ramelteon-treated groups and was accompanied by upregulated ZO-1 and occludin expression. Ramelteon treatment also activated the Nrf2/HO-1 signaling pathway in LPS-induced HPMECs. Furthermore, the addition of ML385 or SnPP reversed the protective effects of ramelteon on LPS-induced oxidative stress, inflammation, apoptosis and cell dysfunction in HPMECs. Collectively, the results suggested that ramelteon alleviated LPS-induced HPMEC damage by activating the Nrf2/HO-1 signaling pathway, making it an effective treatment for ALI.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineCell ProliferationCell SurvivalEndothelial CellsHeme Oxygenase-1HumansIndenesLipopolysaccharidesLungNF-E2-Related Factor 2OccludinOxidative StressSignal TransductionZonula Occludens-1 ProteinAnti-Inflammatory AgentsHeme Oxygenase-1HMOX1 protein, humanIndenesLipopolysaccharidesNFE2L2 protein, humanNF-E2-Related Factor 2OccludinOCLN protein, humanramelteonTJP1 protein, humanZonula Occludens-1 Proteinacute lung injuryapoptosisinflammationlipopolysaccharideRamelteon

Identifiers

PMID34986734
PMCPMC8805948
OpenAlexW4206642625

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.