Fei Mao1, Yunbing Wu1, Xudong Tang2, Juanjuan Wang1, Zhaoji Pan1, Peng Zhang1, Bin Zhang1, Yongmin Yan1, Xu Zhang1, Hui Qian1, Wenrong Xu3. 1. Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of MedicineJiangsu University, 301 Xuefu Road, Zhenjiang, 212013, Jiangsu, People's Republic of China. 2. Jiangsu University of Science and Technology, Zhenjiang, 212018, Jiangsu, People's Republic of China. 3. Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu Province, School of MedicineJiangsu University, 301 Xuefu Road, Zhenjiang, 212013, Jiangsu, People's Republic of China. icls@ujs.edu.cn.
Abstract
OBJECTIVE: To investigate the role of human umbilical cord mesenchymal stem cells (hucMSCs) in the treatment of dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD). RESULTS: ICG-hucMSCs homed to colon tissues of IBD mice 12 h after injection. The injection of hucMSCs significantly relieved the IBD symptoms and inflammatory cell infiltration. The expression of IL-10 gene increased while those of 15-LOX-1, TNF-α, IL-6, IL-1β, and IP-10 genes decreased in colon tissues and spleens of hucMSCs-treated mice. The activation of STAT3 was inhibited in colon tissues and spleens of IBD mice that were treated with hucMSCs. In addition, the percentage of macrophages decreased in colon tissues and spleens of hucMSCs-treated IBD mice. Moreover, we provided evidence that in vitro co-culture with hucMSCs inhibited the expression of 15-LOX-1, IL-6 and p-STAT3 in mouse enterocoelia macrophages. CONCLUSIONS: HucMSCs alleviate DSS-induced IBD through the modulation of 15-LOX-1 in macrophages.
OBJECTIVE: To investigate the role of human umbilical cord mesenchymal stem cells (hucMSCs) in the treatment of dextran sulfate sodium (DSS)-induced inflammatory bowel disease (IBD). RESULTS: ICG-hucMSCs homed to colon tissues of IBD mice 12 h after injection. The injection of hucMSCs significantly relieved the IBD symptoms and inflammatory cell infiltration. The expression of IL-10 gene increased while those of 15-LOX-1, TNF-α, IL-6, IL-1β, and IP-10 genes decreased in colon tissues and spleens of hucMSCs-treated mice. The activation of STAT3 was inhibited in colon tissues and spleens of IBD mice that were treated with hucMSCs. In addition, the percentage of macrophages decreased in colon tissues and spleens of hucMSCs-treated IBD mice. Moreover, we provided evidence that in vitro co-culture with hucMSCs inhibited the expression of 15-LOX-1, IL-6 and p-STAT3 in mouse enterocoelia macrophages. CONCLUSIONS: HucMSCs alleviate DSS-induced IBD through the modulation of 15-LOX-1 in macrophages.