Genipin attenuates dextran sulfate sodium-induced colitis via suppressing inflammatory and oxidative responses.

Autor: Li Z; Department of Gastrointestinal Surgery, The Third Affiliated Hospital of Harbin Medical University, Harbin, China., Ma T; Department of Colorectal Surgery, The Third Affiliated Hospital of Harbin Medical University, Harbin, China., Zhang W; Department of Internal Medicine, The Third Affiliated Hospital of Harbin Medical University, Harbin, China., Shang Y; Department of General Surgery, Pingdingshan Maternal and Child Health Hospital, Henan, China., Zhang Y; Department of Gastrointestinal Surgery, The Third Affiliated Hospital of Harbin Medical University, Harbin, China. zhangyongle@hrbmu.edu.cn., Ma Y; Department of Gastrointestinal Surgery, The Third Affiliated Hospital of Harbin Medical University, Harbin, China. doctormayan@163.com.
Jazyk: angličtina
Zdroj: Inflammopharmacology [Inflammopharmacology] 2020 Feb; Vol. 28 (1), pp. 333-339. Date of Electronic Publication: 2019 Oct 23.
DOI: 10.1007/s10787-019-00639-9
Abstrakt: Genipin is one of the major component in Gardenis fruit, which has long been used in the treatment of many chronic diseases, such as colitis. In the present study, we investigated the protective effects and mechanism of genipin on dextran sodium sulfate (DSS)-induced colitis in mice. Colitis was induced by giving 2.5% (wt/vol) DSS for 7 days. As the results show, DSS-induced body weight loss and colonic histological changes were inhibited by the treatment of genipin. DSS-induced MPO activity, MDA level, TNF-α, and IL-1β production in colonic tissues were also suppressed by genipin. To investigate the mechanism of genipin on DSS-induced colitis, the NF-κB and Nrf2 signaling pathways were detected. The results showed genipin significantly attenuated DSS-induced NF-κB activation and increased the expression of Nrf2 and HO-1 in a dose-dependent manner. The results of the present study indicated that genipin protected mice against colitis through inhibiting inflammatory and oxidative effects.
Databáze: MEDLINE