Astaxanthin protected against the adverse effects induced by diesel exhaust particulate matter via improving membrane stability and anti-oxidative property.

Diesel exhaust particulate matter (DPM), which has been clarified as a Group I carcinogenic agent, is still challenging in its detoxification due to the complex composition and toxic mechanisms. Astaxanthin (AST) is a pleiotropic small biological molecule widely used in medical and healthcare with surprising effects and applications. The present study aimed to investigate the protective effects of AST on DPM-induced injury and the underlying mechanism. Our results indicated that AST significantly suppressed the generation of phosphorylated histone H2AX (γ-H2AX, marker of DNA damage) and inflammation caused by DPM both in vitro and in vivo. Mechanistically, AST prevented the endocytosis and intracellular accumulation of DPM via regulating the stability and fluidity of plasma membranes. Moreover, the oxidative stress elicited by DPM in cells could also be effectively inhibited by AST, together with protecting the structure and function of mitochondria. These investigations provided clear evidence that AST notably reduced DPM invasion and intracellular accumulation by modulating the membrane-endocytotic pathway, which eventually reduced intracellular oxidative stress caused by DPM. Our data might provide a novel clue for curing and treating the harmful effects of particulate matter.