Glabridin attenuates LTA‑induced alveolar macrophage migration via activation of the Nrf2/HO‑1 pathway

Oxidative stress and macrophage migration contribute to chronic inflammation and resultant tissue damage. The nuclear factor erythroid 2‑related factor 2 (Nrf2) antioxidant pathway plays a key role in maintaining redox balance and modulating immune cell behavior. Lipoteichoic acid (LTA), a component of Gram‑positive Bacterial membranes, activates macrophages and overproduces Reactive Oxygen Species (ROS), causing oxidative stress and aberrant macrophage migration. In the present study, the effects of glabridin (GBD), a flavonoid from licorice with antioxidant potential, on LTA‑mediated oxidative stress and alveolar macrophage migration were investigated. GBD pretreatment reduced intracellular ROS levels, as measured through 2',7'‑dichlorofluorescin diacetate and dihydroethidium staining. Immunofluorescence microscopy revealed increased nuclear translocation of Nrf2 following GBD treatment. Western blotting demonstrated elevated expression of Nrf2 and its downstream target, heme oxygenase‑1 (HO‑1). Cotreatment with the Nrf2 inhibitor ML385 attenuated GBD‑mediated Nrf2 activation and HO‑1 expression, suggesting involvement of the Nrf2/HO‑1 pathway. Functionally, GBD inhibited LTA‑induced macrophage migration, and this effect was attenuated by ML385 cotreatment. These findings demonstrate that GBD suppresses LTA‑induced macrophage migration, at least in part, through the Nrf2/HO‑1 signaling pathway, suggesting potential therapeutic relevance in inflammatory lung diseases.

alveolar macrophages; glabridin; lipoteichoic acid; macrophage migration; nuclear factor erythroid 2‑related factor 2/heme oxygenase‑1 pathway.