Prevention of dextran sulfate sodium-induced mouse colitis by the fungal protein Ling Zhi-8 via promoting the barrier function of intestinal epithelial cells. Issue 4 (22nd January 2021)

• Record Type: Journal Article
• Authors: Chen, Yu-Huan; Shin, Jenn-Yeu; Wei, Hsiu-Mei; Lin, Chi-Chien; Yu, Linda C. H.; Liao, Wei-Ting; Chen, Dz-Chi; Chu, Ching-Liang
• Is Part Of: Food & function. Volume 12:Issue 4(2021)
• Page Start: 1639
• Page End: 1650
• Publication Date: 2021-01-22
• Subjects: Food -- Analysis -- Periodicals; Food -- Composition -- Periodicals; Nutrition -- Periodicals; 664.07
• DOI: 10.1039/d0fo02604b
• Languages: English
• ISSNs: 2042-6496

Abstract

Abstract : Protection of intestinal epithelial cells against inflammation by the fungal protein Ling Zhi-8 via maintaining the integrity of tight junctions. Abstract : 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 cells (IECs) is unknown. In this study, we aim to investigate the functional effect of LZ-8 on IECs. LZ-8 effectively rescued the pro-inflammatory cytokine-induced loss of tight junctions (TJs) by enhancing transepithelial electrical resistance (TEER), reducing permeability, and maintaining the distribution of TJ proteins, in Caco-2 cells. Mechanistically, LZ-8 blocked the upregulation of myosin light chain kinase (MLCK) and NF-kB activation by TLR2-mediated suppression of cytokine signaling (SOCS)-1 expression. Furthermore, LZ-8 pre-treatment reduced the pathological scores of dextran sulfate sodium (DSS)-induced colitis in mice. These results indicated that LZ-8 protected the barrier function of IECs against inflammation. Thus, LZ-8 may potentially be a novel candidate for treating inflammatory bowel disease (IBD).