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Updated: Jun 1, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

ROS/SIRT1 signaling mediates mitochondrial dysfunction in hyperoxia-induced BEAS-2B cells injury.

Kun Yang¹, Ting He¹, Rong Zhang¹

¹Department of Neonatology, Children's Medical Center, The Affiliated Hospital of Southwest Medical University, China.

Free Radical Research

|May 30, 2026

Summary

This summary is machine-generated.

Reactive oxygen species (ROS) and sirtuin 1 (SIRT1) play a role in lung injury in preterm infants. Targeting the ROS/SIRT1 pathway may offer new therapeutic strategies for bronchopulmonary dysplasia.

Keywords:

BEAS-2b Hyperoxia SIRT1 mitochondrial injury oxidative stress reactive oxygen species

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Last Updated: Jun 1, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Area of Science:

Cellular and Molecular Biology
Neonatal Medicine
Respiratory Medicine

Background:

Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease in preterm infants.
Its complex pathogenesis necessitates research into cellular and molecular mechanisms.
Understanding the role of reactive oxygen species (ROS) and sirtuin 1 (SIRT1) is crucial.

Purpose of the Study:

To investigate the role of the ROS/SIRT1 axis in hyperoxia-induced injury in BEAS-2B cells.
To explore potential therapeutic targets for BPD at the molecular level.

Main Methods:

BEAS-2B cells were exposed to hyperoxia.
Assays included cell counting kit-8, cell scratch, ROS assay, immunofluorescence, mitochondrial membrane potential assessment, transmission electron microscopy, and Western blot.
The effects of a SIRT1 agonist and an ROS scavenger (N-Acetylcysteine) were evaluated.

Main Results:

Hyperoxia increased ROS and decreased SIRT1 and mitochondria-associated proteins.
SIRT1 activation reduced ROS, improved mitochondrial function, and reversed hyperoxia-induced damage.
ROS scavenging also improved mitochondrial function and reversed molecular changes.

Conclusions:

The ROS/SIRT1 axis is implicated in hyperoxia-induced mitochondrial injury in lung cells.
SIRT1 represents a potential therapeutic target for bronchopulmonary dysplasia.