Propofol alleviates ventilator-induced lung injury through regulating the Nrf2/NLRP3 signaling pathway.

Ventilator-induced lung injury (VILI) causes problems during acute lung injury treatment, and propofol is a well-known drug to prevent VILI. Herein, we discussed how propofol protects against VILI-induced inflammation with the interaction of nuclear factor E2-related factor 2 (Nrf2)/NOD-like receptor protein 3 (NLRP3). We established VILI mouse models for collecting lung tissues, and these mice were later treated with propofol and Nrf2/NLRP3 activator or inhibitor to observe their effects on VILI with inflammatory factors, 8-hydroxy-2 deoxyguanosine, malondialchehyche level, mitochondrial reactive oxygen species production rate, lung wet/dry weight ratio, lung permeability index measured. Propofol treatment improved VILI, alleviated pulmonary inflammation induced by mechanical ventilation. Propofol up-regulated Nrf2 and down-regulated NLRP3 in VILI model. Activating Nrf2 or inhibiting NLRP3 downregulated pro-inflammatory factors in lung tissues in VILI mice. Above all, we can conclude that propofol exerts it protective function against VILI and the subsequent inflammatory responses through activating Nrf2 and inhibiting NLRP3 expression. Therefore, Nrf2 activator and NLRP3 inhibitor might be latent targets in the VILI prevention.