Astaxanthin protects tilapia head kidney cells against polystyrene microplastics-induced inflammation through MAPK and NF-κB signaling pathways

Abstract

Microplastic particles (MPs) are emerging as global pollutants, causing oxidative stress and inflammation in aquaculture. Astaxanthin is classified as a xanthophyll carotenoid compound with many functions, including anti-inflammatory properties. However, astaxanthin has yet to be proven to counteract the proinflammatory effects of MPs. In this study, we used the polystyrene (PS)-MPs-treated Nile tilapia (Oreochromis niloticus) head kidney cells as a model to explore the anti-inflammatory effect of astaxanthin. In primary cell cultures from the head kidney, the administration of PS-MPs dose-dependently inhibited cell viability, whereas the application of astaxanthin negated the viability-suppressive effect of PS-MPs by inhibiting the cellular reactive oxygen species (ROS) production. Furthermore, astaxanthin treatment repressed PS-MPs-induced interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) secretion. In parallel studies, the inhibitory effects of PS-MPs on these cytokines release were prevented by the p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinases (ERK1/2), and nuclear factor-kappa B (NF-κB) inhibitors. However, the c-Jun N-terminal kinase (JNK1/2) inhibition did not influence cytokines secretion in PS-MPs-treated head kidney cells. Using Western blot analysis, we demonstrated that astaxanthin dose-dependently inhibited the PS-MPs-induced stimulation of phosphorylation of the p38 MAPK, ERK1/2, and Iκκα/β. Additionally, astaxanthin noticeably prevented PS-MPs-induced NF-κB nuclear accumulation. These findings suggest that astaxanthin can repair PS-MPs-triggered inflammatory responses in tilapia head kidney cells via downregulating the MAPK (p38 MAPK and ERK1/2) and NF-κB signaling pathways.