Abstract

Five potential polysaccharides from guava seed (GSPS), common buckwheat (CBPS), bitter buckwheat (BBPS), red Formosa lambsquarters (RFLPS), and yellow Formosa lambsquarters (YFLPS) were selected to measure their effects on mouse peritoneal macrophages in the absence or presence of lipopolysaccharide (LPS). Macrophage-conditioned media (MCM) in the absence or presence of 5 selected polysaccharides were prepared to treat MCF-7 cells. The cell viability was determined using 3-(4,5-dimethylthiazol-2-diphenyl)-2,5-tetrazolium bromide (MTT) assay. Proinflammatory (also known as M1 type) (interleukin- (IL-) 1β, IL-6 and tumor necrosis factor- (TNF-) α) and anti-inflammatory (also known as M2 type) (IL-10) cytokines secreted by macrophages were determined using ELISA. The relationship between MCF-7 cell growth and M1/M2 cytokine secretion profiles in the corresponding MCM were delineated. The results showed that 5 selected polysaccharides, except BBPS, significantly (P < 0.05) and dose-dependently increased M1 (IL-1β + IL-6 + TNF-α)/M2 (IL-10) cytokine secretion ratios by macrophages in the absence of LPS, suggesting that four selected polysaccharides have M1 polarization property. However, all of 5 selected polysaccharides significantly (P < 0.05) decreased proinflammatory (IL-1β + IL-6 + TNF-α)/anti-inflammatory (IL-10) cytokine secretion ratios by LPS-stimulated macrophages, exhibiting that all of the 5 selected polysaccharides, particularly GSPS, have anti-inflammatory potential. All MCM prepared with these selected polysaccharides (except YFLPS) significantly enhanced their inhibitory effects on MCF-7 cell growth. A negative correlation was noted between MCF-7 cell viabilities and M1/M2 cytokine secretion ratios ((IL-6 + TNF-α)/IL-10) in the corresponding MCM, suggesting that increases in M1 macrophages in the tumor microenvironment might inhibit MCF-7 cell growth. Particular polysaccharides including RFLPS, GSPS, YFLPS, and CBPS may increase the percentage of M1 macrophages in the tumor environment and further inhibit MCF-7 cell growth via immunotherapy.

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