Evidence map›Paper›PMID 36926276›Full record

ArticleJournal of inflammation research2023

Pretreatment with Eupatilin Attenuates Inflammation and Coagulation in Sepsis by Suppressing JAK2/STAT3 Signaling Pathway.

Yilun Lu, Ding Li, Yueyue Huang, Yuanyuan Sun, Hongmin Zhou, Fanrong Ye, Hongjing Yang, Tingting Xu, Shichao Quan, Jingye Pan

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.0field-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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. 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

10 authors at 1 institution in 1 country.

Yilun Lu *Department of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.ORCID 0000-0003-2318-9865
Ding Li *Department of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.ORCID 0000-0002-9149-4362
Yueyue HuangDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Yuanyuan SunDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Hongmin ZhouDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Fanrong YeDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Hongjing YangDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Tingting XuDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Shichao QuanWenzhou Key Laboratory of Critical Care and Artificial Intelligence, Wenzhou, People's Republic of China.
Jingye PanDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Wenzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Sepsis is an aggressive and life-threatening organ dysfunction induced by infection. Excessive inflammation and coagulation contribute to the negative outcomes for sepsis, resulting in high morbidity and mortality. In this study, we explored whether Eupatilin could alleviate lung injury, reduce inflammation and coagulation during sepsis. Methods: We constructed an in vitro sepsis model by stimulating RAW264.7 cells with 1 μg/mL lipopolysaccharide (LPS) for 6 hours. The cells were divided into control group, LPS group, LPS+ Eupatilin (Eup) group, and Eup group to detect their cell activity and inflammatory cytokines and coagulation factor levels. Cells in LPS+Eup and Eup group were pretreated with Eupatilin (10μM) for 2 hours. In vivo, mice were divided into sham operation group, cecal ligation and puncture (CLP) group and Eup group. Mice in the CLP and Eup groups were pretreated with Eupatilin (10mg/kg) for 2 hours by gavage. Lung tissue and plasma were collected and inflammatory cytokines, coagulation factors and signaling were measured. Results: In vitro, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and tissue factor (TF) expression in LPS-stimulated RAW264.7 cells was downregulated by Eupatilin (10μM). Furthermore, Eupatilin inhibited phosphorylation of the JAK2/STAT3 signaling pathway and suppressed p-STAT3 nuclear translocation. In vivo, Eupatilin increased the survival rate of the mice. In septic mice, plasma concentrations of TNF-α, IL-1β and IL-6, as well as TF, plasminogen activator inhibitor 1 (PAI-1), D-dimer, thrombin-antithrombin complex (TAT) and fibrinogen were improved by Eupatilin. Moreover, Eupatilin alleviated lung injury by improving the expression of inflammatory cytokines and TF, fibrin deposition and macrophage infiltration in lung tissue. Conclusion: Our results revealed that Eupatilin may modulate inflammation and coagulation indicators as well as improve lung injury in sepsis via the JAK2/STAT3 signaling pathway.

Indexed as

coagulationEupatilininflammationJAK2/STAT3sepsis

Identifiers

PMID36926276
PMCPMC10013575
OpenAlexW4323852960

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.