Evidence map›Paper›PMID 29694408›Full record

ArticlePloS one2018

Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway.

Ying Lu, Ting Yu, Jingyao Liu, Lina Gu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-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

32 citing papers in PubMed, 68 citations in OpenAlex.

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  14. Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  15. Beneficial Role of Vitexin in Parkinson's Disease.The Malaysian journal of medical sciences : MJMS · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Anti-Inflammatory Effects of Phytochemical Components ofMolecules (Basel, Switzerland) · 2022
    Review
  20. 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

4 authors at 2 institutions in 1 country.

Ying LuIntensive Care Unit, the First Hospital of Jilin University, Changchun, China.
Ting YuDepartment of Nutrition, the Second Hospital of Jilin University, Changchun, China.
Jingyao LiuDepartmen of Neurology, the First Hospital of Jilin University, Changchun, China.
Lina GuIntensive Care Unit, the First Hospital of Jilin University, Changchun, China.ORCID 0000-0001-7239-6057
Jilin University · CNSecond Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA major feature of acute lung injury (ALI) is excessive inflammation in the lung. Vitexin is an active component from medicinal plants which has antioxidant and anti-inflammatory activities. Oxidative stress and inflammation play important roles in the pathophysiological processes in ALI. In the current study, we investigate the effect and potential mechanisms of Vitexin on lipopolysaccharide (LPS)-induced ALI.

methodsALI was induced by LPS intratracheal instillation in C57BL/6 wild-type mice and Nrf2 gene knocked down (Nrf2-/-) mice. One hour before LPS challenge, Vitexin or vehicle intraperitoneal injection was performed. Bronchoalveolar lavage fluid and lung tissues were examined for lung inflammation and injury at 24 h after LPS challenge.

resultsOur animal study's results showed that LPS-induced recruitment of neutrophils and elevation of proinflammatory cytokine levels were attenuated by Vitexin treatment. Vitexin decreased lung edema and alveolar protein content. Moreover, Vitexin activated nuclear factor erythroid-2-related factor 2 (Nrf2), and increased the activity of its target gene heme oxygenase (HO)-1. The LPS-induced reactive oxygen species were inhibited by Vitexin. In addition, the activation of the nucleotide-binding domain and leucine-rich repeat PYD-containing protein 3 (NLRP3) inflammasome was suppressed by Vitexin. However, these effects of Vitexin were abolished in the Nrf2-/- mice. Our cell studies showed that Vitexin enhanced the expression of Nrf2 and HO-1 activity. Moreover, reactive oxygen species (ROS) and IL-1β productions were reduced in Vitexin-treated cells. However, knockdown of Nrf2 by siRNA in RAW cells reversed the benefit of Vitexin.

conclusionsVitexin suppresses LPS-induced ALI by controlling Nrf2 pathway.

Indexed as

Acute Lung InjuryAnimalsAnti-Inflammatory AgentsApigeninBronchoalveolar Lavage FluidHeme Oxygenase-1Interleukin-1betaLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutNeutrophilsNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressAnti-Inflammatory AgentsApigeninHeme Oxygenase-1Interleukin-1betaLipopolysaccharidesNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesRNA, Small Interferingvitexin

Identifiers

PMID29694408
PMCPMC5942793
OpenAlexW2802534073

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.