Immunomodulatory effects of seed peptide lunasin in RAW264.7 macrophages in obese microenvironments

In 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 adipocyteconditioned 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 & PRIME;,7 & PRIME;-dichlorodihydrofluorescein diacetate (DCF-DA) staining, 28% of nitric oxide production, and 27% of tumor necrosis factor-& alpha; 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.

Automated summary

This study investigated the mechanism of lunasin in regulating immune functions of RAW264.7 macrophages under obesity-related conditions. The findings showed that lunasin protected the vitality of macrophages, suppressed leptin secretion, and reduced inflammation markers in LPS-stimulated co-culture. However, it had opposing effects in adipocyte-conditioned medium and co-culture without LPS. Additionally, lunasin enhanced phagocytosis in both LPS and adipocyte-conditioned medium challenges.