Sulforaphane attenuates oxidative stress and inflammation induced by fine particulate matter in human bronchial epithelial cells

Abstract

• Sulforaphane alleviated oxidative damages induced by PM2.5 exposure. • Sulforaphane attenuated PM2.5-induced inflammatory responses. • Sulforaphane may be a promising bioactive against PM2.5-related health effects. • Sulforaphane relieved PM-related damages through activation of Nrf2/Keap1 pathway. PM2.5 can directly damage human lungs and affect overall health worldwide. Oxidative stress and inflammation play critical roles in the toxicity of PM2.5. Sulforaphane, a phytochemical mainly derived from cruciferous vegetables, possesses anti-oxidative and anti-inflammatory efficacy. The objective of this work is to evaluate the protective effects of sulforaphane against damages induced by PM2.5 in human bronchial epithelial (HBE) cells and investigate the physiochemical properties of PM2.5. The results revealed that PM2.5 were mainly fine particles abundant in transition metals and PAHs, partly responsible for the excess generation of reactive oxygen species (ROS). Moreover, PM2.5 exposure resulted in oxidative damages and inflammatory responses in cells. However, pretreatment with sulforaphane significantly alleviated these negative effects, probably through the nuclear factor E2 related factor 2/antioxidant responsive element (Nrf2/ARE) pathway. Collectively, these findings demonstrate that pretreatment with sulforaphane ameliorates PM2.5-induced cell injury through the suppression of oxidative stress and inflammation in HBE cells.