Evidence map›Paper›PMID 31375092›Full record

ArticleBMC complementary and alternative medicine2019

Triptolide attenuates lipopolysaccharide-induced inflammatory responses in human endothelial cells: involvement of NF-κB pathway.

Chundong Song, Youping Wang, Lin Cui, Fengna Yan, Si Shen

Open access · goldAbstract read
In one paragraph

Article in BMC complementary and alternative medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 3% 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, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. Review of OxLDL Driven Inflammatory Cell Activation.Current atherosclerosis reports · 2025
    Pooled it
  2. Pooled it
  3. Review
  4. Article
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  7. Review
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  9. Article
  10. Vascular Protective Effects ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
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  12. Article
  13. Article
  14. Triptolide improves myocardial fibrosis in rats through inhibition of nuclear factor kappa B and NLR family pyrin domain containing 3 inflammasome pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    Article
  15. Article
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  17. Study of the Active Components and Molecular Mechanism ofFrontiers in molecular biosciences · 2021
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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

5 authors at 1 institution in 1 country.

Chundong SongCentral Laboratory and Department of Pediatrics Division of Cardiology First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, 450000, China.
Youping WangCentral Laboratory and Department of Pediatrics Division of Cardiology First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, 450000, China. wangyp8@163.com.
Lin CuiCentral Laboratory and Department of Pediatrics Division of Cardiology First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, 450000, China.
Fengna YanCentral Laboratory and Department of Pediatrics Division of Cardiology First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, 450000, China.
Si ShenCentral Laboratory and Department of Pediatrics Division of Cardiology First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, 450000, China.
Henan University of Traditional Chinese Medicine · CN

Funding

Henan Provincial Science and Technique Foundation for International Cooperation Program 162102410048National Nature Science Foundation of China 81673734 & 81170243Science and Technique Foundation from the Education Department of Henan Province 2010B360012
6 · The paper itself

Abstract

backgroundEndothelial cell inflammation is a central event in the pathogenesis of numerous cardiovascular diseases, including sepsis and atherosclerosis. Triptolide, a principal bioactive ingredient of Traditional Chinese Medicine Tripterygium wilfordii Hook.F., displays anti-inflammatory actions in vivo. However, the mechanisms underlying these beneficial effects remain undetermined. The present study investigated the effects and possible mechanisms of triptolide on lipopolysaccharide (LPS)-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs).

methodsThe effects of triptolide on the LPS-induced production and expression of inflammatory molecules, monocyte adhesion and activation of nuclear factor (NF)-κB pathway were examined in cultured HUVECs.

resultsIn cultured HUVECs, pre-treatment with triptolide dose-dependently attenuated LPS-induced cytokine and chemokine production, adhesion molecule expression and monocyte adhesion. Mechanistically, triptolide was found to dose-dependently inhibit the LPS-induced increases in the DNA binding activity of NF-κB p65 associated with attenuating IκBα phosphorylation and its degradation. Additionally, the present study revealed that triptolide inhibited LPS-triggered NF-κB transcriptional activation in a dose-dependent manner.

conclusionsThe results of the present study indicated that triptolide suppresses the inflammatory response of endothelial cells possibly via inhibition of NF-κB activation.

Indexed as

Anti-Inflammatory AgentsDiterpenesDrugs, Chinese HerbalEpoxy CompoundsHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMonocytesNF-kappa BNF-KappaB Inhibitor alphaPhenanthrenesTripterygiumTumor Necrosis Factor-alphaAnti-Inflammatory AgentsDiterpenesDrugs, Chinese HerbalEpoxy CompoundsLipopolysaccharidesNF-kappa BNF-KappaB Inhibitor alphaPhenanthrenestriptolideTumor Necrosis Factor-alphaEndothelial cellsInflammationLipopolysaccharideNuclear factor-κBTriptolide

Identifiers

PMID31375092
PMCPMC6679459
OpenAlexW2965724806

What OpenQuestion holds

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Registered trials

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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.