Α-Lipoic acid attenuates silica-induced pulmonary fibrosis through maintenance of iron homeostasis and improving mitochondrial function in airway epithelial cells.

Iron metabolism disorders cause pulmonary epithelial cell damage during silicosis-induced fibrosis. It was found that α-lipoic acid (ALA) contributes to iron homeostasis and inhibition of oxidative stress. Therefore, it is necessary to investigate whether ALA attenuates silica-induced pulmonary fibrosis by regulating iron metabolism and improving mitochondrial function in airway epithelial cells. In the present study, the mechanism of action and effect of ALA on silicosis-induced fibrosis were illustrated using immunofluorescence (IF) staining, inductively coupled plasma mass spectrometry (ICP-MS), western blotting, and reverse transcription quantitative polymerase chain reaction (RT-qPCR). The results demonstrated that ALA alleviated pulmonary fibrosis by maintaining iron homeostasis and protecting the mitochondria in bronchial epithelial lung cells. The findings obtained herein revealed that iron metabolism disorders are involved in SiO2-induced pulmonary fibrosis, and that ALA alleviates SiO2-induced ferroptosis, maintains the iron metabolic balance and protects the mitochondria in airway epithelial cells.