Propofol modulates Nrf2/NLRP3 signaling to ameliorate cigarette smoke-induced damage in human bronchial epithelial cells.

ABSTRACT

Cigarette smoke extract (CSE) is known as a significant contributor to chronic obstructive pulmonary disease (COPD). Propofol, an anesthetic agent, has been studied for its potential protective effects against lung damage. This study aimed to elucidate the protective mechanisms of propofol against CSE-induced damage in human bronchial epithelial 16HBE cells. In CSE-induced 16HBE cells treated by propofol with or without transfection of nuclear factor erythroid 2-related factor 2 (Nrf2) interference plasmids, CCK-8 assay and lactate dehydrogenase (LDH) assay evaluated cytotoxicity. TUNEL assay and Western blot appraised cell apoptosis. ELISA and relevant assay kits severally measured inflammatory and oxidative stress levels. DCFH-DA fluorescent probe detected intracellular reactive oxygen species (ROS) activity. Immunofluorescence staining and Western blot estimated pyroptosis. Also, Western blot analyzed the expression of Nrf2/NLR family pyrin domain containing 3 (NLRP3) signaling-related proteins. Propofol was found to enhance the viability, reduce LDH release, and alleviate the apoptosis, inflammatory response, oxidative stress and pyroptosis in CSE-induced 16HBE cells in a concentration-dependent manner. Meanwhile, propofol decreased NLRP3 expression while raised Nrf2 expression. Further, after Nrf2 was silenced, the impacts of propofol on Nrf2/NLRP3 signaling, LDH release, apoptosis, inflammatory response, oxidative stress and pyroptosis in CSE-exposed 16HBE cells were eliminated. Conclusively, propofol may exert protective effects against CSE-induced damage in 16HBE cells, partly through the modulation of the Nrf2/NLRP3 signaling pathway, suggesting a potential therapeutic role for propofol in CSE-induced bronchial epithelial cell damage.