Prevention of dextran sulfate sodium-induced mouse colitis by the fungal protein Ling Zhi-8 via promoting the barrier function of intestinal epithelial cells.
作者： Ching-Liang Chu , Yu-Huan Chen , Jenn-Yeu Shin , Hsiu-Mei Wei , Chi-Chen Lin
DOI: 10.1039/D0FO02604B
关键词: Inflammation 、 Cytokine 、 Barrier function 、 Fungal protein 、 Immune system 、 Chemistry 、 Cell biology 、 Colitis 、 Myosin light-chain kinase 、 Tight junction
摘要: The fungal immunomodulatory protein Ling Zhi-8 (LZ-8) isolated from Ganoderma lucidum (GL) regulates immune cells and inhibits tumor growth; however, the role of LZ-8 in protecting intestinal epithelial (IECs) is unknown. In this study, we aim to investigate functional effect on IECs. effectively rescued pro-inflammatory cytokine-induced loss tight junctions (TJs) by enhancing transepithelial electrical resistance (TEER), reducing permeability, maintaining distribution TJ proteins, Caco-2 cells. Mechanistically, blocked upregulation myosin light chain kinase (MLCK) NF-kB activation TLR2-mediated suppression cytokine signaling (SOCS)-1 expression. Furthermore, pre-treatment reduced pathological scores dextran sulfate sodium (DSS)-induced colitis mice. These results indicated that protected barrier function IECs against inflammation. Thus, may potentially be a novel candidate for treating inflammatory bowel disease (IBD).
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