Evidence map›Paper›PMID 29398669›Full record

ArticleExperimental animals2018

Anti-inflammatory effect of tranexamic acid against trauma-hemorrhagic shock-induced acute lung injury in rats.

Yue Teng, Cong Feng, Yunen Liu, Hongxu Jin, Yan Gao, Tanshi Li

Open access · diamondAbstract read
In one paragraph

Article in Experimental animals, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
2.4field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Efficacy of Tranexamic Acid on GABANeurochemical research · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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 at 2 institutions in 1 country.

Yue TengDepartment of Emergency Medicine, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, P.R. China.
Cong FengDepartment of Emergency Medicine, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, P.R. China.
Yunen LiuDepartment of Emergency Medicine, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang 110016, P.R. China.
Hongxu JinDepartment of Emergency Medicine, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang 110016, P.R. China.
Yan GaoDepartment of Emergency Medicine, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang 110016, P.R. China.
Tanshi LiDepartment of Emergency Medicine, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, P.R. China.
Chinese PLA General Hospital · CNGeneral Hospital of Shenyang Military Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been demonstrated that tranexamic acid (TXA), a synthetic derivative of lysine, alleviates lung damage in a trauma-hemorrhagic shock (T/HS) model. Nevertheless, the mechanism of TXA against acute lung injury (ALI) has not deeply elaborated. In this study, we generated a T/HS rat model based on previous research, and TXA (50 mg/kg and 100 mg/kg) was intravenously injected into these rats prior to or post T/HS. The results revealed that the decreased survival rate and impaired lung permeability of the rats caused by T/HS were improved by TXA pretreatment or posttreatment. T/HS-triggered over-generation of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in bronchoalveolar fluid and serum was inhibited by TXA, and the enzymatic activity of myeloperoxidase (MPO) in lung tissues was suppressed by TXA as well. Furthermore, TXA treatment deactivated the poly ADP-ribose polymerase-1 (PARP1)/nuclear factor κB (NF-κB) signaling pathway in the lungs of T/HS rats, as evidenced by increased IκBα expression, and decreased cleaved PARP1, p-p65 (Ser276), p-p65 (Ser529), p-IκBα (ser32/ser36), and intercellular adhesion molecule-1. While the expression level of total p65 did not change after T/HS, its DNA binding activity was strengthened. Both TXA pretreatment and posttreatment suppressed this effect on the DNA binding activity of NF-κB. Taken together, our results reveal that administration of TXA effectively relieves T/HS-induced ALI, at least in part, by attenuating the abnormal pulmonary inflammation.

Indexed as

Anti-Inflammatory AgentsMolecular Targeted TherapyAcute Lung InjuryAnimalsBronchoalveolar Lavage FluidDisease Models, AnimalDNAInfusions, IntravenousInterleukin-6LungMaleNeoplasm ProteinsNF-kappa BNucleocytoplasmic Transport ProteinsPeroxidasePoly (ADP-Ribose) Polymerase-1Anti-Inflammatory AgentsDNAInterleukin-6Neoplasm ProteinsNF-kappa BNucleocytoplasmic Transport Proteinsp65 oncofetal mRNA transport protein, ratParp1 protein, ratPeroxidasePoly (ADP-Ribose) Polymerase-1Tranexamic AcidTumor Necrosis Factor-alphaacute lung injuryhemorrhagic shockinflammationNF-κBtranexamic acid

Identifiers

PMID29398669
PMCPMC6083028
OpenAlexW2789189490

What OpenQuestion 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 OpenQuestion graph.