Quercetin Attenuates Cadmium-Induced Acute Lung Injury via Nrf2-Keap1 Pathway Activation

Cadmium, a toxic heavy metals that would cause lung tissue damage and structural alterations via oxidative stress and inflammatory responses. This study was designed to investigate the protective function and its potential mechanism of quercetin against cadmium-induced acute lung injury. Rat and BEAS-2B cell models of CdCl₂-induced ALI were established, and the apoptotic and proliferative activities of tissue cells, inflammatory factors such as TNF-α, IL-6, and IL-1β, and the expression of key proteins in the Nrf2-Keap1 pathway, mitochondrial pathway, and mitochondrial membrane potential were examined using Immunohistochemistry, TUNEL, CCK8, ELISA, Western blot, and flow cytometry to evaluate the therapeutic effect of quercetin. Quercetin significantly alleviated CdCl₂-induced pulmonary edema, tissue damage and inflammatory response, and inhibited lung cell Apoptosis in rats. It increased the expression of antioxidant enzyme genes, reduced ROS generation, restored Redox Equilibrium, and protected mitochondrial function by the Nrf2-Keap1 signaling pathway activation. In addition, quercetin also exhibited inhibitory effects on CdCl₂-induced Apoptosis in BEAS-2B cells in vitro. Quercetin significantly attenuated cadmium-induced acute lung injury through antioxidant stress and protection of mitochondrial function, and has potential therapeutic value for acute lung injury.

acute lung injury; apoptosis; cadmium; oxidative stress; quercetin.