Astaxanthin attenuates proinflammatory signaling and promotes adipogenesis in human adipose stem cells.

Adipose tissues not only store and release energy but also function as endocrine organs and maintaining adipose stem cells (ASCs) and functional adipocytes is essential for systemic metabolic health. Astaxanthin (Ast), an oxygenated carotenoid enriched in seafood, is recognized as a bioactive compound known for its anti-inflammatory and antioxidative properties. However, limited information is available regarding the roles of Ast in human ASCs (hASCs). This study examined the capacity of Ast to counteract TNFα actions in the inflammatory signaling pathways and proliferation of hASCs. The effects of Ast on hASC adipogenesis and the underlying mechanisms were also determined. Proliferation rates were measured with an MTT assay, and adipogenesis was determined by measuring the expression levels of adipogenic markers and lipid accumulation. Ast (0.01-10 μM) had no effect under basal conditions but attenuated TNFα-mediated suppression of cell viability, as well as activation of canonical proinflammatory signaling pathways in hASCs. Lower concentrations of Ast (0.01 and 0.1 μM) increased adipogenesis, while higher concentrations (2 and 10 μM) inhibited adipogenesis. Ast (0.01 and 0.1 μM) induced adipogenesis by suppressing the anti-adipogenic Wnt/β-catenin pathway and upregulating the adipogenic transcription factors, C/EBPα and PPARγ, during the early periods of adipogenesis. Our results suggest that Ast has beneficial impacts on adipose tissue by suppressing inflammation, thereby maintaining the pool of adipose progenitors and promoting their adipogenesis.