An absolute interlinks between inflammation and obesity with scarce investigations on the role of lutein in inflammation-induced obesity motivated us to explore the protective mechanism of lutein on adipogenesis-mediated inflammation in vitro by culturing RAW264.7 macrophages in adipocyte conditioned medium. The RAW264 macrophage cells were cultured with adipocyte-conditioned media, and the potency of lutein on the expression of adipocyte inflammation-associated protein markers (IL-1β, MCP-1, TNF-α, IL-6, NF-κB, and IKKα/β) were analyzed by western blotting. The data revealed that lutein effectively reduces the protein levels of major inflammatory markers such as NF-κB, IL-1β, MCP-1, and TNF-α in differentiated adipocytes. Interestingly, lutein hampered inflammation in the RAW264 cells that were cultured in adipocyte-conditioned media by lowering the protein expression of IL-1β, MCP-1, and TNF-α. The blockage of inflammation by lutein in both differentiated adipocytes, and adipogenesis-induced macrophages is associated with suppression of IKK α/β phosphorylation. These data suggest that lutein potentially alters adipocyte differentiation-mediated inflammation by regulating the NF-κB signaling pathway. Thus, lutein could be utilized as a potent nutraceutical agent in the management of obesity and associated inflammation. PRACTICAL APPLICATIONS: Lutein isolated from a dietary source exhibited an inhibitory effect in adipogenesis-induced inflammations. The findings of this study authenticate the diversified prospective of lutein in regulating obesity and other inflammation-related diseases. Thus, it is understood that continuous intake of lutein-rich food or dietary intervention of lutein may reduce the risk of developing obesity.
Keywords: NF-κB signaling; adipogenesis; inflammation; lutein; macrophages.
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