Evidence map›Paper›PMID 30251233›Full record

ArticleInflammopharmacology2019

Anti-inflammatory effects of Chinese propolis in lipopolysaccharide-stimulated human umbilical vein endothelial cells by suppressing autophagy and MAPK/NF-κB signaling pathway.

Hongzhuan Xuan, Wenwen Yuan, Huasong Chang, Minmin Liu, Fuliang Hu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The antimicrobial activity of propolis extract onJournal of medical microbiology · 2025
    Article
  4. Propolis: A Natural Substance with Multifaceted Properties and Activities.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Antibacterial activity of Chinese propolis and its synergy with β-lactams against methicillin-resistant Staphylococcus aureus.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022
    Article
  8. Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
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 2 institutions in 1 country.

Hongzhuan XuanSchool of Life Science, Liaocheng University, Liaocheng, 252059, China. hongzhuanxuan@163.com.ORCID http://orcid.org/0000-0002-7823-1488
Wenwen YuanSchool of Life Science, Liaocheng University, Liaocheng, 252059, China.
Huasong ChangSchool of Life Science, Liaocheng University, Liaocheng, 252059, China.
Minmin LiuSchool of Life Science, Liaocheng University, Liaocheng, 252059, China.
Fuliang HuCollege of Animal Sciences, Zhejiang University, Hangzhou, 310029, China. flhu@zju.edu.cn.
Liaocheng University · CNZhejiang University · CN

Funding

National Natural Science Foundation of China 31201860National Natural Science Foundation of China 31672499
6 · The paper itself

Abstract

This study aimed to investigate the possible benefits of Chinese poplar propolis (CP) in inhibiting inflammation using vascular endothelial cells (VECs) cultured in a nutrient-rich condition exposed to lipopolysaccharide (LPS). Cell proliferation was detected by sulforhodamine B assay and EdU kit. The production of reactive oxygen species (ROS) and level of mitochondrial membrane potential were determined with fluorescent probe DCHF and JC-1, respectively. Protein expression was examined by immunofluorescence staining and western blotting. The results showed that CP (6.25, 12.5, and 25 μg/mL) significantly reduced LPS-induced cytotoxicity, and when challenged with CP substantially suppressed ROS overproduction and protected mitochondrial membrane potential. CP treatment significantly inhibited autophagy by inhibiting LC3B distribution and accumulation, and elevating the p62 level in an mTOR-independent manner but mainly by suppressing the translocation of p53 from the cytoplasm to the nucleus. Furthermore, CP treatment markedly reduced protein levels of TLR4 at 12 and 24 h and significantly suppressed nuclear translocation of NF-κB p65 from cytoplasm to nucleus. In addition, CP treatment significantly reduced the phosphorylation of JNK, ERK1/2, and p38 MAPK. Our findings demonstrated that CP protects VECs from LPS-induced oxidative stress and inflammation, which might be associated with depressing autophagy and MAPK/NF-κB signaling pathway. The results provided novel insights for the potential use of nutrient-rich propolis against inflammation.

Indexed as

Anti-Inflammatory AgentsAutophagyCell LineCell ProliferationHumansHuman Umbilical Vein Endothelial CellsInflammationLipopolysaccharidesMAP Kinase Signaling SystemMembrane Potential, MitochondrialNF-kappa Bp38 Mitogen-Activated Protein KinasesPropolisReactive Oxygen SpeciesSignal TransductionTranscription Factor RelAAnti-Inflammatory AgentsLipopolysaccharidesNF-kappa Bp38 Mitogen-Activated Protein KinasesPropolisReactive Oxygen SpeciesTranscription Factor RelATumor Suppressor Protein p53Anti-inflammatoryAutophagyChinese propolisReactive oxygen speciesToll-like receptor 4

Identifiers

PMID30251233
OpenAlexW2893225667

What OpenQuestion holds

Textmetadata
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.