ZnO nanoparticles act as supportive therapy in DSS-induced ulcerative colitis in mice by maintaining gut homeostasis and activating Nrf2 signaling

• Published in: Scientific reports Vol. 7; no. 1; p. 43126
• Main Authors: Li, Jinquan, Chen, Hanqing, Wang, Bing, Cai, Chengxu, Yang, Xu, Chai, Zhifang, Feng, Weiyue
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 24.02.2017; Nature Publishing Group
• Subjects: 13/1; 13/21; 631/92; 64/60; 692/4017; 82/1; Antioxidants; Cancer; Colon; Dextran; Dextran sulfate; Gastrointestinal tract; Health problems; Homeostasis; Humanities and Social Sciences; IL-1β; Inflammatory bowel disease; Inflammatory bowel diseases; Inflammatory diseases; Intestine; Malondialdehyde; multidisciplinary; Nanoparticles; Peroxidase; Remission; Rodents; Science; Sodium; Sulfates; Tumor necrosis factor; Ulcerative colitis
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep43126

Inflammatory bowel diseases (IBD) are widespread inflammatory diseases that cause debilitating health problems including cancer. In this study, we show that ZnO nanoparticle (ZnONP) treatment has markedly dose-dependent effects on the remission of dextran sulfate sodium (DSS)-induced ulcerative colitis in mice. We demonstrate the mechanism involves the antioxidant and anti-inflammatory abilities of ZnONPs to suppress ROS and malondialdehyde (MDA) production; increase GSH level; suppress proinflammatory cytokines IL-1β and TNF-α and myeloperoxidase (MPO). The ZnONP treatment is able to activate the Nrf2 pathway in the cellular antioxidant defense system. The novel finding is that ZnONP combined with mesalazine (5-ASA) can enhance the therapeutic efficacy of 5-ASA in the treatment of DSS-induced colitis. Lastly, we found that ZnONP treatment can restore the changes in special colonic bacteria of DSS-mice while the drug 5-ASA cannot. These results indicate that ZnONPs can act as a medical additive for the therapy of IBD.