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

Bronchopulmonary dysplasia is a common chronic lung disease in preterm infants with a complex pathogenesis, and it is necessary to search for the potential pathogenesis and therapeutic strategies of bronchopulmonary dysplasia at the cellular molecular level. The present study investigated the role of reactive oxygen species (ROS)/sirtuin 1 (SIRT1) axis in hyperoxia-induced BEAS-2B cells injury.

Cell counting kit-8, cell scratch, ROS assay, immunofluorescence, mitochondrial membrane potential, transmission electron microscopy assay and Western blot were performed to investigate the impairment of BEAS-2B by hyperoxia as well as the roles of SIRT1 and ROS in hyperoxia-induced BEAS-2B injury.

(1) Hyperoxia increased ROS in a time-dependent manner and decreased the levels of SIRT1 and mitochondria-associated proteins in BEAS-2B. (2) The SIRT1 agonist reduced ROS and improved mitochondrial membrane potential levels, attenuated mitochondrial fragmentation and mitochondrial morphological damage, and reversed the hyperoxia-induced decrease in mitochondria-associated proteins expression in BEAS-2B. (3) The ROS scavenger N-Acetylcysteine reduced ROS levels, improved mitochondrial membrane potential levels, attenuated mitochondrial morphological damage, and reversed the hyperoxia-induced decrease in SIRT1 and mitochondria-associated proteins levels in BEAS-2B.

The ROS/SIRT1 axis is involved in hyperoxia-induced mitochondrial injury in BEAS-2B cells, and SIRT1 may be a potential therapeutic target for bronchopulmonary dysplasia.