Characterization of immunostimulatory pectic polysaccharide isolated from leaves of Diospyros kaki Thumb. (Persimmon). (October 2016)

• Record Type: Journal Article
• Authors: Shin, Myoung-Sook; Lee, Ho; Hong, Hee-Do; Shin, Kwang-Soon
• Is Part Of: Journal of functional foods. Volume 26(2016)
• Page Start: 319
• Page End: 329
• Publication Date: 2016-10
• Subjects: Diospyros kaki Thumb. leaves -- Polysaccharide -- Macrophage activation -- MAPK -- NF-κB; MAPK mitogen-activated protein kinases -- NF-κB nuclear factor kappa-light-chain-enhancer of activated B cells -- JNK c-Jun N-terminal kinases -- ERK extracellular signal-regulated kinases -- p38 p38 mitogen-activated protein kinases -- iNOS inducible nitric oxide synthase; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2016.07.025
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: We isolated three polysaccharide fractions from Diospyros kaki Thumb. leaves. Their molecular weight, chemical properties and sugar compositions were analysed. The isolated fraction (PLE-I) stimulate immune activity in murine macrophages. The mechanism relies mainly on the JNK/ERK-c-Jun pathways. Abstract: In this study, three polysaccharide fractions (PLE-I–III) were purified from crude polysaccharides from leaves of Diospyros kaki Thumb. (Persimmon) that were hydrolysed with pectinase, and their monosaccharide composition was analysed . Among the three fractions, PLE-I was found to markedly stimulate the immune activity (IL-6/IL-12 and TNF-α production) of peritoneal macrophages cells. Signal transduction studies showed that PLE-I phosphorylated MAPK and NF-κB in RAW264.7 cells in a concentration-dependent manner. The effect of PLE-I on IL-6 production was found to be completely suppressed by specific inhibitors of JNK (SP) and ERK (U0126), but not a p38 inhibitor. Moreover, PLE-I-induced phosphorylation of the transcription factor c-Jun was inhibited by SP and U0126 treatment, whereas iNOS expression was blocked by inhibitors of JNK, p38, and NF-κB. Collectively, these results suggest that PLE-I-induced macrophage activation is regulated via JNK/ERK and not p38, whereas iNOS expression is primarily regulated via MAPK and NF-κB.