Evidence map›Paper›PMID 40028157›Full record

ArticleFrontiers in pharmacology2025

Cordycepin attenuates NLRP3/Caspase-1/GSDMD-mediated LPS-induced macrophage pyroptosis.

Zige Liu, Li Lv, Jiao Wei, Yuli Xie, Mujia Jili, Yian Huang, Rirong Yang, Yu Luo

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. MnOMaterials today. Bio · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. 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

8 authors.

Zige Liu *Center for Genomic and Personalized Medicine, Guangxi key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, University Engineering Research Center of Digital Medicine and Healthcare, Guangxi Medical University, Nanning, Guangxi, China.
Li Lv *Department of Physiology, School of Basic Medical Sciences, Nanning, Guangxi, China.
Jiao WeiDepartment of Physiology, School of Basic Medical Sciences, Nanning, Guangxi, China.
Yuli XieCenter for Genomic and Personalized Medicine, Guangxi key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, University Engineering Research Center of Digital Medicine and Healthcare, Guangxi Medical University, Nanning, Guangxi, China.
Mujia JiliCenter for Genomic and Personalized Medicine, Guangxi key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, University Engineering Research Center of Digital Medicine and Healthcare, Guangxi Medical University, Nanning, Guangxi, China.
Yian HuangCenter for Genomic and Personalized Medicine, Guangxi key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, University Engineering Research Center of Digital Medicine and Healthcare, Guangxi Medical University, Nanning, Guangxi, China.
Rirong YangCenter for Genomic and Personalized Medicine, Guangxi key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, University Engineering Research Center of Digital Medicine and Healthcare, Guangxi Medical University, Nanning, Guangxi, China.
Yu LuoDepartment of Clinical Laboratory, Guangxi Academy of Medical Sciences, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyroptosis, a form of programmed cell death driven by the NLRP3 inflammasome, is a key contributor to inflammation in various diseases. This study aimed to investigate the anti-inflammatory mechanisms of cordycepin, focusing on its role in macrophage pyroptosis. Molecular docking analysis was performed to evaluate the binding affinity of cordycepin to key pyroptosis-related proteins, including NLRP3, Caspase-1, and GSDMD. RAW264.7 cells were pre-treated with cordycepin to assess its effects on pyroptosis. Key measurements included reactive oxygen species (ROS) levels, xanthine oxidase (XO) activity, and the expression of NLRP3, Caspase-1, and GSDMD. Additionally, lactate dehydrogenase (LDH) release, interleukin (IL)-1β and IL-18 levels in the culture supernatant, and macrophage cell death rates were evaluated using Hoechst 33342/PI dual staining. The results demonstrated that cordycepin exhibits strong binding affinity for NLRP3, Caspase-1, and GSDMD. Cordycepin pre-treatment significantly reduced ROS levels and XO activity, inhibited the expression of NLRP3, cleaved-Caspase-1, and cleaved-GSDMD, and decreased pyroptosis-associated inflammatory cytokines IL-1β and IL-18, along with Caspase-1 activity. Furthermore, cordycepin reduced the macrophage pyroptosis rate. In conclusion, cordycepin inhibits macrophage pyroptosis by reducing XO activity, suppressing ROS production, and regulating the expression of key molecules in the NLRP3/Caspase-1/GSDMD pathway. These findings provide a strong experimental basis for the potential development of cordycepin as a novel anti-inflammatory agent.

Indexed as

cordycepinLPSmacrophagemacrophage pyroptosisRAW 264.7

Identifiers

PMID40028157
PMCPMC11868043

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.