Huang, Pei YingPei YingHuangCHIA-CHIEN HSIEH2023-08-282023-08-282023-09-0117564646https://scholars.lib.ntu.edu.tw/handle/123456789/634759In adiposity, immune cells infiltrate adipose tissues, especially macrophages, forming chronic inflammation. This study aimed to investigate the mechanism of lunasin regulating immune functions of RAW264.7 macrophages in obesity-related conditions. Lipopolysaccharide (LPS) triggered an acute inflammation, and adipocyte-conditioned medium (Ad-CM) and co-cultures of RAW264.7 macrophages and 3T3-L1 adipocytes were used to mimic obese microenvironments. Lunasin protected the vitality of RAW cells and suppressed leptin secretion in Ad-CM. In LPS, lunasin reduced 47% of 2′,7′-dichlorodihydrofluorescein diacetate (DCF-DA) staining, 28% of nitric oxide production, and 27% of tumor necrosis factor-α secretion in LPS-stimulated co-culture, while there were opposing effects in Ad-CM and co-culture without LPS. Moreover, LPS-stimulated migration was inhibited at 44% by lunasin, while Ad-CM-declined 49% of migration. Lunasin increased 21% and 42% of phagocytosis in LPS and Ad-CM challenges. Overall, the study first revealed that lunasin exerted immunomodulation in macrophages against LPS-stimulated inflammation but boosted immune functions in obesity-related microenvironments.enAdipocyte | Immunomodulation | Inflammation | Lunasin | Macrophagesjournal article10.1016/j.jff.2023.1057192-s2.0-85167416413https://api.elsevier.com/content/abstract/scopus_id/85167416413