Flower extract of Caragana sinica. ameliorates Dss-induced ulcerative colitis by affecting TLR4/NF-κB and TLR4/MAPK signaling pathway in a mouse model
نویسندگان
1 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
2 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
3 Yunnan Institute of Food Safety, Kunming University of Science and Technology, Kunming, 650500, People’s Republic of China
4 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
5 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
6 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
7 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
8 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
9 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
10 College of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, 650500, People’s Republic of China
doi
10.22038/ijbms.2021.53847.12106چکیده
Objective(s): This study aimed to find out the protective effects and preliminary mechanisms of the flower extract of Caragana sinica (FEC) on dextran sulfate sodium salt (DSS)-induced colitis.Materials and Methods: The ulcerative colitis models of mice induced by 3% DSS were established and treated with FEC. Body weight changes, disease activity index (DAI), colon histopathological score, anti-oxidant ability, and the level of inflammatory cytokines were determined. The expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) were assessed in colonic tissue by immunohistochemical staining. Western blot was used to analyze the expression of TLR4/ nuclear factor kappa-B (NF-κB) and TLR4/ mitogen-activated protein kinase (MAPK) signaling pathway-related proteins. Results: FEC significantly prevented body weight loss and colonic shortening and reduced the disease activity index and histopathological score (p <0.05). Moreover, FEC treatment remarkably down-regulated the levels of myeloperoxidase (MPO), interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) and up-regulated the levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and interleukin 10 (IL-10) in the colon of DSS mice (p <0.05). Furthermore, the expression of TLR4/NF-κB and TLR4/MAPK pathway-related proteins was inhibited by FEC (p <0.05). Conclusion: Our findings demonstrated that FEC could serve as a potential therapeutic agent for treatment of ulcerative colitis.
