Evidence map›Paper›PMID 40110767›Full record

ArticleThoracic cancer2025

Diosmetin Inhibits NETs Formation in Neutrophils Through Regulating Nrf2 Signaling.

Lijuan Guo, Hongyang Luo, Yuxin Lei, Leiyan Gu, Yaohui Wang, Siyuan Wang, Zihan Lian, Yuhao Li, Yanlan Xiang, Guanhua Du and 9 more

Abstract read
In one paragraph

Article in Thoracic cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Veterinary sciences · 2026
    Article
  2. Review
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

19 authors.

Lijuan GuoDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Hongyang LuoDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yuxin LeiDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Leiyan GuDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yaohui WangDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Siyuan WangDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Zihan LianDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yuhao LiDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yanlan XiangDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Guanhua DuDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Rui ShaoState Key Laboratory of Component-Based Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Xiaoxuan TianState Key Laboratory of Chinese Medicine Modernization, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Han ZhangState Key Laboratory of Component-Based Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Linjie ShenDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Junli ChenDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Yi WangDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Ning HuangDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.
Xiaoyu NiuDepartment of Obstetrics and Gynecology, Key Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
Jingyu LiDepartment of Pathophysiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, Sichuan, China.ORCID https://orcid.org/0000-0003-0997-9115

Funding

Foundation of State Key Laboratory of Component-based Chinese Medicine CBCM2020205National Key Research and Development Program of China 2021YFC2009100National Natural Science Foundation of China 31401188Sichuan Association for Science and Technology 2018RCTJ04the Natural Science Foundation of Sichuan Provine 2022NSFSC0834
6 · The paper itself

Abstract

backgroundNeutrophil extracellular traps (NETs) are important pieces of equipment for neutrophils. Excess NETs play promoting roles in cancer-associated thrombosis (CAT). Therefore, directing NETs formation is a promising therapeutic strategy in thrombosis and related diseases. Diosmetin, an antioxidant flavonoid derived from dietary sources, might be involved in NETs formation and CAT.

methodsFirstly, the tests of cell-free DNA and Immunofluorescence were applied to evaluate the NETs levels of neutrophils. Luminol-based chemiluminescence and the DCFH-DA probe were used to detect the levels of reactive oxygen species (ROS) in neutrophils. Then, network pharmacological analysis and molecular docking were used to predict potential target molecules of diosmetin. The RT-qPCR was performed to measure the levels of Nrf2 and HO-1. A series of functional assays of neutrophils were used to examine the effect of diosmetin on other neutrophil functions. Finally, an animal model of deep vein thrombosis was constructed to assess the effect of diosmetin on thrombosis.

resultsDiosmetin reduced NETs and ROS levels in neutrophils. Then, molecular mechanisms analysis suggested that Nrf2 might be the primary target of diosmetin. Diosmetin treatment increased the levels of Nrf2 and HO-1 in NETs-generating neutrophils. An inhibitor of Nrf2 diminished the negative effect of diosmetin on NETs generation. Lastly, the murine thrombosis model results indicated that diosmetin treatment reduced thrombosis via NETs formation.

conclusionDiosmetin exerts as anti-NETs effect through Nrf2 signaling in neutrophils, showing the therapeutic potential in thromboembolism and related pathological processes, such as CAT.

Indexed as

Extracellular TrapsFlavonoidsFlavonolsNeutrophilsNF-E2-Related Factor 2AnimalsDisease Models, AnimalHumansMaleMiceReactive Oxygen SpeciesSignal TransductiondiosmetinFlavonoidsFlavonolsNFE2L2 protein, humanNF-E2-Related Factor 2Reactive Oxygen SpeciesdiosmetinNETsNrf2thrombosis

Identifiers

PMID40110767
PMCPMC11923709

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.