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Role and Molecular Mechanism of Farnesoid X Receptor(FXR) and RIPK3 in the Formation of Acute Respiratory Distress Syndrome in Neonates

NCT02598648 · Status: UNKNOWN · Phase: NA · Type: INTERVENTIONAL · Enrollment: 40

Last updated 2022-10-14

No results posted yet for this study

Summary

In the clinical data, the changes of RIPK3 and FXR were monitored in the lung lavage fluid and blood from the patients.

In vivo experiments to find high risk factors to induce AEC necrosis and further lead to ARDS evidence, can provide a more direct theoretical research foundation for the pathogenesis of ARDS.

Conditions

  • Acute Respiratory Distress Syndrome
  • Acute Lung Injury
  • FXR
  • RIPK3

Interventions

OTHER

FXR

FXR could elevate the transcription of RIPK3, a key protein in necroptosis, and play important role in bile aicd induced alveolar epithelial cell(AEC) necroptosis. FXR were measured in neonate with ALI、ARDS and control

OTHER

RIPK3

FXR(farnesoid-X-receptor) could elevate the transcription of RIPK3, a key protein in necroptosis, and play important role in bile aicd induced alveolar epithelial cell(AEC) necroptosis. RIPK3 were measured in neonate with ALI、ARDS and control.

Sponsors & Collaborators

  • Daping Hospital and the Research Institute of Surgery of the Third Military Medical University

    lead OTHER

Principal Investigators

  • Hu Zh Xue, Doctorate · Daping Hospital and the Research Institute of Surgery of the Third Military Medical University

Study Design

Allocation
NON_RANDOMIZED
Purpose
DIAGNOSTIC
Masking
NONE
Model
PARALLEL

Eligibility

Max Age
1 Week
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2015-09-20
Primary Completion
2023-09-30
Completion
2023-09-30

Countries

  • China

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02598648 on ClinicalTrials.gov