Evidence map›Paper›PMID 29257294›Full record

ArticleMolecular medicine reports2018

Baicalein protects against endothelial cell injury by inhibiting the TLR4/NF‑κB signaling pathway.

Chun-Xia Wan, Man Xu, Si-Hui Huang, Qing-Qing Wu, Yuan Yuan, Wei Deng, Qi-Zhu Tang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 19 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

7 authors at 1 institution in 1 country.

Chun-Xia WanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, P.R. China.
Man XuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, P.R. China.
Si-Hui HuangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, P.R. China.
Qing-Qing WuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, P.R. China.
Yuan YuanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, P.R. China.
Wei DengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, P.R. China.
Qi-Zhu TangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, Hubei 430060, P.R. China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The involvement of vascular endothelial injury with the pathophysiological process of heart failure has been identified. Baicalein (BAI), a flavonoid extracted from the root of Scutellaria baicalensis, is reported to exert antibacterial, antiviral, antithrombotic and antioxidant effects. The aim of the present study was to investigate the effects of BAI on lipopolysaccharide (LPS)‑induced vascular endothelial injury. Human umbilical vein endothelial cells (HUVECs) were stimulated by LPS (10 µM) in the presence or absence of BAI. The expressions of the inflammatory cytokines interleukin (IL)‑lβ, IL‑6, tumor necrosis factor‑α (TNF‑α) and monocyte chemoattractant protein‑1 (MCP‑1) were analyzed by reverse transcription‑quantitative polymerase chain reaction, western blotting and enzyme‑linked immunosorbent assay. Cell apoptosis was assessed by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The results showed that BAI significantly inhibited the LPS‑induced inflammatory response and apoptosis in HUVECs. BAI suppressed the LPS‑induced upregulation of IL‑1β, IL‑6, TNF‑α and MCP‑1. Furthermore, BAI decreased the expression of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and cleaved caspase‑3; however, it increased the protein level of Bcl‑2. The inhibitory effect of BAI may occur through the suppression of the Toll‑like receptor 4 (TLR4)/phosphorylated (p)‑transforming growth factor β‑activated kinase 1/tumor necrosis factor receptor‑associated family member associated nuclear factor (NF)‑κB activator‑binding kinase 1 (p‑TBK1)/NF‑κB signaling pathway. An increase in the level of p‑TBK1 by MRT67307 abolished the effect of BAI on p‑p65. In conclusion, the results of the present research suggested that BAI ameliorated endothelial cell injury associated with TLR4/NF‑κB signaling, and highlighted the potential clinical use of BAI in blocking endothelial dysfunction and preventing heart failure.

Indexed as

Anti-Inflammatory AgentsAntioxidantsApoptosisEndothelial CellsFlavanonesHumansHuman Umbilical Vein Endothelial CellsInflammationLipopolysaccharidesNF-kappa BScutellaria baicalensisSignal TransductionToll-Like Receptor 4Anti-Inflammatory AgentsAntioxidantsbaicaleinFlavanonesLipopolysaccharidesNF-kappa BTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID29257294
PMCPMC5783530
OpenAlexW2772387559

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.