Evidence map›Paper›PMID 32575718›Full record

ArticleMolecules (Basel, Switzerland)2020

Epigallocatechin-3-Gallate (EGCG), an Active Compound of Green Tea Attenuates Acute Lung Injury Regulating Macrophage Polarization and Krüpple-Like-Factor 4 (KLF4) Expression.

Saleh A Almatroodi, Ahmad Almatroudi, Mohammed A Alsahli, Mohammad A Aljasir, Mansoor Ali Syed, Arshad Husain Rahmani

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.8field-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

34 citing papers in PubMed, 62 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 2 countries.

Saleh A AlmatroodiDepartment of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 52571, Saudi Arabia.
Ahmad AlmatroudiDepartment of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 52571, Saudi Arabia.ORCID 0000-0002-1491-6402
Mohammed A AlsahliDepartment of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 52571, Saudi Arabia.
Mohammad A AljasirDepartment of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 52571, Saudi Arabia.ORCID 0000-0002-3708-9200
Mansoor Ali SyedTranslational Research Lab, Department of Biotechnology, Faculty of Natural Sciences, Jamia Millia Islamia, New Delhi 110025, India.ORCID 0000-0003-2697-7832
Arshad Husain RahmaniDepartment of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 52571, Saudi Arabia.
Qassim University · SADepartment of Biotechnology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are serious clinical complications with a high frequency of morbidity and mortality. The initiation and amplification of inflammation is a well-known aspect in the pathogenesis of ALI and related disorders. Therefore, inhibition of the inflammatory mediators could be an ideal approach to prevent ALI. Epigallocatechin-3-gallate (EGCG), a major constituent of green tea, has been shown to have protective effects on oxidative damage and anti-inflammation. The goal of the present study was to determine whether EGCG improves phenotype and macrophage polarisation in LPS-induced ALI. C57BL/6 mice were given two doses of EGCG (15 mg/kg) intraperitoneally (IP) 1 h before and 3 h after LPS instillation (2 mg/kg). EGCG treatment improved histopathological lesions, Total Leucocyte count (TLC), neutrophils infiltration, wet/dry ratio, total proteins and myeloperoxidase (MPO) activity in LPS-induced lung injury. The results displayed that EGCG reduced LPS-induced ALI as it modulates macrophage polarisation towards M2 status. Furthermore, EGCG also reduced the expression of proinflammatory M1 mediators iNOS TNF-α, IL-1β and IL-6 in the LPS administered lung microenvironment. In addition, it increased the expression of KLF4, Arg1 and ym1, known to augment the M2 phenotype of macrophages. EGCG also alleviated the expression of 8-OHdG, nitrotyrosine, showing its ability to inhibit oxidative damage. TREM1 in the lung tissue and improved lung regenerative capacity by enhancing Ki67, PCNA and Ang-1 protein expression. Together, these results proposed the protective properties of EGCG against LPS-induced ALI in may be attributed to the suppression of M1/M2 macrophages subtype ratio, KLF4 augmentation, lung cell regeneration and regulating oxidative damage in the LPS-induced murine ALI.

Indexed as

8-Hydroxy-2'-DeoxyguanosineAcute Lung InjuryAnimalsAnti-Inflammatory AgentsArginasebeta-N-AcetylhexosaminidasesCatechinCell ProliferationInterleukin-1betaInterleukin-6Ki-67 AntigenKruppel-Like Factor 4Kruppel-Like Transcription FactorsLectinsLipopolysaccharidesMacrophages3-nitrotyrosine8-Hydroxy-2'-DeoxyguanosineAnti-Inflammatory AgentsArg1 protein, mouseArginasebeta-N-AcetylhexosaminidasesCatechinChil3 protein, mouseepigallocatechin gallateInterleukin-1betaInterleukin-6Ki-67 AntigenKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsLectinsLipopolysaccharidesNitric Oxide Synthase Type IINos2 protein, mousePeroxidaseProliferating Cell Nuclear AntigenTeaTREM1 protein, mouseTriggering Receptor Expressed on Myeloid Cells-1Tumor Necrosis Factor-alphaTyrosineacute lung injuryepigallocatechin-3-gallate (EGCG)macrophage polarisation

Identifiers

PMID32575718
PMCPMC7356789
OpenAlexW3036040297

What OpenQuestion holds

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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.