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Acetylation of polysaccharide from Morchella angusticeps peck enhances its immune activation and anti-inflammatory activities in macrophage RAW264.7 cells
- Yang, Yaxuan, Chen, Jinlong, Lei, Lin, Li, Fuhua, Tang, Yu, Yuan, Ya, Zhang, Yueqiao, Wu, Surui, Yin, Ran, Ming, Jian
- Food and chemical toxicology 2019 v.125 pp. 38-45
- IKappaB kinase, Morchella, acetylation, anti-inflammatory activity, cell proliferation, cell viability, drugs, functional foods, inducible nitric oxide synthase, lipopolysaccharides, macrophages, nitric oxide, signal transduction, toxicology, transcription factor NF-kappa B, tumor necrosis factor-alpha, ultraviolet-visible spectroscopy
- Morchella angusticeps Peck has been recognized as a resource of nutraceuticals and drug discovery. Three acetylated polysaccharides (Ac-PMEP1-3) with appropriate degree of substitution were obtained from Morchella angusticeps Peck, chemically characterized, and cultured with macrophage RAW264.7 cells to evaluate their immune activation and anti-inflammatory activities. Results of ultraviolet–visible spectroscopy and fourier-transform infrared showed these modifications were successful. Compared with the control group, PMEP and Ac-PMEP1-3 enhanced cell proliferation and the production of nitric oxide and tumor necrosis factor-α of RAW264.7 macrophages (cultured without lipopolysaccharide). Compared with PMEP, Ac-PMEP3 enhanced cell viability and NO production by inducing the degradation of cytoplasmic IκBα and nuclear translocation of NF-κB subunit p65 as well as the expression of iNOS and phosphorylated-p38. Moreover, in lipopolysaccharide-stimulated RAW264.7 macrophages, Ac-PMEP3 showed a stronger ability to suppress the overproduction of nitric oxide and tumor necrosis factor-α by down-regulating the level of nuclear NF-κB p65, iNOS, and phosphorylated-p38 and inhibiting the degradation of cytoplasmic IκBα. Therefore, Ac-PMEP enhanced immune activation and anti-inflammatory activities via nuclear factor κB and p38/mitogen-activated protein kinase signaling pathways.