Selective effects of ginseng pectins on galectin-3-mediated T cell activation and apoptosis

• Published in: Carbohydrate polymers 2019-09, Vol.219, p.121-129
• Main Authors: Xue, Huiting, Zhao, Zihan, Lin, Zhiying, Geng, Jie, Guan, Yuan, Song, Chengcheng, Zhou, Yifa, Tai, Guihua
• Format: Article
• Language: English
• Subjects: Anti-tumor; Galectin-3; Inhibitor; Pectin; T-cell activation; T-cell apoptosis
• ISSN: 0144-8617; 1879-1344
• DOI: 10.1016/j.carbpol.2019.05.023

•Ginseng pectins inhibit Gal-3-induced T-cell apoptosis and signaling pathways.•Ginseng pectins do not affect Gal-3-induced T-cell activation.•Ginseng pectins partially preserve activation signaling pathways.•Ginseng pectins promote T-cell function and inhibit tumor growth. Galectin-3 (Gal-3) can induce T-cell activation and apoptosis and plays a role in tumor immune tolerance. Here, we demonstrate that ginseng pectins selectively inhibit Gal-3-induced T-cell apoptosis, while not affecting T-cell activation. This finding stands in contrast to that from the use of modified citrus pectin (MCP) and potato galactan (P-galactan) that inhibit both. Whereas PKC/ERK and ROS/ERK pathways are involved in both T-cell activation and apoptosis, the Ras/PI3K/Akt pathway is unique to T-cell activation. Ginseng pectins selectively inhibit the ROS/ERK pathway. Using the Sarcomar-180 mouse model in which Gal-3 expression is increased, we found that ginseng pectins (but not MCP or P-galactan) significantly promote T-cell proliferation and IL-2 expression, and inhibit tumor growth by 45%. These in vivo data correlate well with selective effects of pectins on Gal-3-mediated T-cell apoptosis and activation. Our study suggests a novel approach for the development of polysaccharide-based agents that target Gal-3 function.