Administration of geniposide ameliorates dextran sulfate sodium-induced colitis in mice via inhibition of inflammation and mucosal damage

被引:42
作者
Zhang, Zecai [1 ]
Li, Yanxin [1 ]
Shen, Peng [1 ]
Li, Shan [1 ]
Lu, Xiaojie [1 ]
Liu, Jiuxi [1 ]
Cao, Yongguo [1 ]
Liu, Bo [1 ]
Fu, Yunhe [1 ]
Zhang, Naisheng [1 ]
机构
[1] Jilin Univ, Coll Vet Med, Changchun 130062, Jilin, Peoples R China
基金
中国国家自然科学基金;
关键词
Geniposide; Colitis; Caco-2; cells; Inflammation; Intestinal barrier; ACTIVATED-RECEPTOR-GAMMA; ULCERATIVE-COLITIS; BOWEL DISEASES; ENDOTHELIAL-CELLS; AGONIST; PATHOGENESIS; CYTOKINES; MEDICINE; PATHWAY; CANCER;
D O I
10.1016/j.intimp.2017.05.033
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Ulcerative colitis (UC), an idiopathic inflammatory bowel disease, not only affects millions of patients worldwide, but also increases the risk of colon cancer. Geniposide is an iridoid glycoside and has many biological activities such as anti-inflammatory and antioxidant. However, its protective efficacy and mechanism of action against UC are still unclear. In this study, we aimed to investigate the protective effects and mechanisms of geniposide on dextran sulfate sodium (DSS)-induced experimental colitis in mice. The results revealed that geniposide alleviated body weight loss, disease activity index, colon length shortening and colonic pathological damage induced by DSS. Geniposide significantly suppressed pro-inflammatory cytokines by regulating NF-xti and PPAR gamma pathways in vivo and in vitro. Furthermore, geniposide also significantly regulated the expressions of ZO-1 and occludin in DSS-induced experimental colitis in mice and lipopolysaccharide (LPS)-triggered inflammation in Caco-2 cells. These findings indicated that geniposide may be a new natural chemopreventive agent to combat UC.
引用
收藏
页码:168 / 177
页数:10
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