Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a recurrent and progressively aggravating autoimmune disease. Serum ANCA are pathogenic antibodies in AAV, such as myeloperoxidase (MPO)-ANCA and proteinase 3 (PR3)-ANCA. The kidneys and lungs are the most commonly involved organs, and patients often present with crescentic glomerulonephritis and pulmonary haemorrhage [1]. Although patient therapeutic efficacy has improved in recent years with the clinical use of immunosuppressive agents and biologics, new treatment strategies are needed to minimize the side effects of therapy and improve the quality of life of patients with AAV.

The pathogenesis of AAV is associated with chronic inflammation, imbalance of oxidative stress, and immune dysregulation. Neutrophils are central to the pathogenesis of AAV. Activated by lipopolysaccharide, complement, or pro-inflammatory factors in infection or inflammation, neutrophils could aggregate, deform, and induce a respiratory burst that undergoes degranulation and releases neutrophil extracellular traps (NETs) [2], [3]. AAV patients produced auto-antibodies against the contents in NETs, such as MPO and PR3. In turn, ANCA stimulated neutrophils to further activate and release NETs, various enzymes, cytokines, and reactive oxygen species (ROS) leading to further inflammation and endothelial injury [4], [5]. Therefore, regulating inflammation and oxidative stress to maintain homeostasis of the organism's immuno-inflammatory microenvironment is crucial for AAV treatment.

Astaxanthin is a lipid-soluble carotenoid derived mainly from marine organisms with powerful antioxidant and anti-inflammatory capacity [6]. Studies in vitro have shown that ATX could decrease the production of superoxide anion, H2O2, IL-6, and TNF-α by neutrophils [7], [8]. Meantime, ATX can increase the ratio of glutathione (GSH) /L-Glutathione oxidized (GSSH) in rats and enhance the antioxidant capacity of plasma [9]. In addition, Lu et al. found that low molecular weight heparin-ATX nanoparticles could reduce neutrophil recruitment, inhibit the formation of NETs, and thus suppress breast cancer metastasis [10]. Therefore, we hypothesize that ATX might have a protective role in the pathogenesis of AAV.