Diesel exhaust particles induced blood-brain barrier dysfunction through inflammation, oxidative stress, and activation of the RhoA/ROCK signaling pathway

Diesel Exhaust Particles (DEPs) emitted by diesel engines represent a substantial contributor to ambient particulate matter. Extensive research has demonstrated that DEPs pose significant risks to human health. This study seeks to elucidate the molecular mechanisms underlying DEPs-induced dysfunction of the blood-brain barrier (BBB). The research team exposed bEND.3 cells to various concentrations of DEPs for 24 h and evaluated parameters including cell morphology, viability, inflammatory markers, oxidative stress, tight junction protein expression, and modulation of the RhoA/ROCK signaling pathway. The findings revealed that DEPs exposure resulted in morphological and ultrastructural alterations, elevated apoptosis rates, and reduced cell viability. Additionally, DEPs stimulated the release of pro-inflammatory cytokines, induced oxidative stress, disrupted tight junction protein expression, increased BBB permeability, and activated the RhoA/ROCK signaling pathway, thereby amplifying these deleterious effects. Collectively, our results demonstrate that DEPs impair BBB functionality through a cascade of cellular injury mechanisms. These findings highlight the profound impact of air pollution on the central nervous system and underscore the urgent need for stringent regulations on diesel emissions to protect brain health, particularly among populations in urban areas with high exposure to traffic-related emissions.