Evidence map›Paper›PMID 39219424›Full record

ArticleCurrent pharmaceutical biotechnology2025

The Effect of Hydroxysafflor Yellow A on Inflammatory Injury in LPS-induced Endothelial Cell Injury Model through TLR4/NF-κB Pathway Based on Network Pharmacology and Experimental Verification.

Qinghua Guo, Xiaoyan Zhu, Xiaoyang Zhang, Xu Wang, Feida Fu, Wandong She

Abstract read
PubMed Publisher
In one paragraph

Article in Current pharmaceutical biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

6 authors.

Qinghua GuoDepartment of Otolaryngology-Head and Neck Surgery, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210008, China.
Xiaoyan ZhuDepartment of Otolaryngology-Head and Neck Surgery, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210008, China.
Xiaoyang ZhangDepartment of Central Laboratory, Nanjing Integrated Traditional Chinese and Western Medicine Hospital Affiliated with Nanjing University of Chinese Medicine, Nanjing, 210014, China.
Xu WangDepartment of Otolaryngology, Nanjing integrated traditional Chinese and Western Medicine Hospital Affiliated with Nanjing University of Chinese Medicine, Nanjing, 210014, China.
Feida FuDepartment of Otolaryngology, Nanjing integrated traditional Chinese and Western Medicine Hospital Affiliated with Nanjing University of Chinese Medicine, Nanjing, 210014, China.
Wandong SheDepartment of Otolaryngology-Head and Neck Surgery, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210008, China.

Funding

Jiangsu Provincial Administration of Traditional Chinese Medicine, China YB2020032Nanjing Medical Science and Technology Development Key project, China ZKX-21012Nanjing Medical Science and Technology Development program, China YKK185Natural Science Funds of Jiangsu province, China BK20231122Special Fund for Clinical Research of Nanjing Drum Tower Hospital, China 2022-LCYJ-MS-01
6 · The paper itself

Abstract

objectiveThe objective of this study is to search for hydroxysafflor yellow A (HSYA) and Idiopathic sudden sensorineural hearing loss (ISSNHL)-related target genes and to study the treatment effects of HSYA on lipopolysaccharide (LPS)-induced endothelial cell injury.

methodsWe used network pharmacology to screen molecules related to HSYA and ISSNHL, then analyzed these molecules and their enriched biological processes and signaling pathways via Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). We selected inflammation-related hub genes for molecular docking determination by protein-protein interaction (PPI) analysis, and further verified them with

resultsThirty-four HSYA-ISSNHL-related differential genes were obtained using drug-disease differential gene screening using online tools. Three key proteins, NF-κB, CASP3, and MAPK1, were selected according to Degree > 20. Among them, NF-κB is closely related to inflammation and ISSNHL. In

conclusionHSYA may reduce inflammation and oxidative stress by inhibiting the expression of the TLR4 / NF-κB-related signaling pathway, therefore protecting endothelial cells, which might be a potential mechanism of HSYA in ISSNHL treatment.

Indexed as

Anti-Inflammatory AgentsChalconeEndothelial CellsInflammationNF-kappa BQuinonesToll-Like Receptor 4HumansLipopolysaccharidesMolecular Docking SimulationNetwork PharmacologyOxidative StressProtein Interaction MapsSignal TransductionAnti-Inflammatory AgentsChalconehydroxysafflor yellow ALipopolysaccharidesNF-kappa BQuinonesTLR4 protein, humanToll-Like Receptor 4endothelial cellshydroxysafflor pigment Alipopolysaccharidemolecular dockingNetwork pharmacologyTLR4 / NF-κB.

Identifiers

PMID39219424

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.