Evidence map›Paper›PMID 31756053›Full record

ArticleJournal of cellular and molecular medicine2020

Genistein-3'-sodium sulphonate protects against lipopolysaccharide-induced lung vascular endothelial cell apoptosis and acute lung injury via BCL-2 signalling.

Lei Yi, Mengling Chang, Quanming Zhao, Zengding Zhou, Xiaoqin Huang, Feng Guo, Jingning Huan

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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

7 authors at 3 institutions in 1 country.

Lei YiDepartment of Burn and Plastic Surgery, School of Medicine, Ruijin Hospital, Shanghai Jiao Tong University, Shanghai, China.
Mengling ChangDepartment of Burn and Plastic Surgery, School of Medicine, Ruijin Hospital, Shanghai Jiao Tong University, Shanghai, China.
Quanming ZhaoDepartment of Orthopedic Surgery, The Second Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.
Zengding ZhouDepartment of Burn and Plastic Surgery, School of Medicine, Ruijin Hospital, Shanghai Jiao Tong University, Shanghai, China.
Xiaoqin HuangDepartment of Burn and Plastic Surgery, School of Medicine, Ruijin Hospital, Shanghai Jiao Tong University, Shanghai, China.
Feng GuoDepartment of Plastic Surgery, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Jingning HuanDepartment of Burn and Plastic Surgery, School of Medicine, Ruijin Hospital, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0003-0905-2774
Shanghai Jiao Tong University · CNNantong University · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Under septic conditions, Lipopolysaccharide (LPS)-induced apoptosis of lung vascular endothelial cells (ECs) triggers and aggravates acute lung injury (ALI), which so far has no effective therapeutic options. Genistein-3'-sodium sulphonate (GSS) is a derivative of native soy isoflavone, which has neuro-protective effects through its anti-apoptotic property. However, whether GSS protects against sepsis-induced lung vascular endothelial cell apoptosis and ALI has not been determined. In this study, we found that LPS-induced Myd88/NF-κB/BCL-2 signalling pathway activation and subsequent EC apoptosis were effectively down-regulated by GSS in vitro. Furthermore, GSS not only reversed the sepsis-induced BCL-2 changes in expression in mouse lungs but also blocked sepsis-associated lung vascular barrier disruption and ALI in vivo. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on Myd88/NF-κB/BCL-2 signalling in lung ECs.

Indexed as

Acute Lung InjuryAnimalsApoptosisEndothelium, VascularGenisteinLipopolysaccharidesLungMaleMiceMice, Inbred C57BLPhytoestrogensProtective AgentsProto-Oncogene Proteins c-bcl-2Bcl2 protein, mouseGenisteinLipopolysaccharidesPhytoestrogensProtective AgentsProto-Oncogene Proteins c-bcl-2acute lung injuryapoptosisendothelial cellsgenistein-3′-sodium sulphonatesepsis

Identifiers

PMID31756053
PMCPMC6933390
OpenAlexW2990060464

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.