Antioxidation and anti-inflammatory actions of the extract of Nitraria Tangutorum Bobr. fruits reduce the severity of ulcerative colitis in a dextran sulphate sodium-induced mice model

抗氧化剂 化学 超氧化物歧化酶 石油醚 过氧化氢酶 谷胱甘肽 免疫印迹 生物化学 药理学 传统医学 色谱法 生物 医学 萃取(化学) 基因
作者
Qiuping Zou,Jian Feng,Ting Li,Gui-Guang Cheng,Weiguang Wang,Gaoxiong Rao,Hongping He,Yulin Li
出处
期刊:Journal of Functional Foods [Elsevier]
卷期号:91: 105005-105005 被引量:1
标识
DOI:10.1016/j.jff.2022.105005
摘要

• 25 compounds were characterized from the extracted of Nitraria Tangutorum Bobr. fruits by using UHPLC-ESI-HRMS/MS method. • All extracts exhibited antioxidant activity and enhanced the activities of antioxidant enzymes in HepG-2 cells. • CE presented the highest phenolics, and has the best antioxidant and anti-inflammatory effects in vivo and in vitro. • CE reduced weight loss and the disease activity in DSS-induced UC mice. • CE inhibited the activation of MAPK/NF- κ B signaling pathways. In the present study, we characterised 25 compounds in the extract of Nitraria Tangutorum Bobr. fruits by using the HPLC/MS/MS method. We determined the antioxidant activities of ethanol, petroleum ether, chloroform (CE), ethyl acetate, n-butanol, and water extracts of N. Tangutorum fruits. All extracts were found to exhibit the antioxidant activity and significantly enhance the activities of antioxidant enzymes in H 2 O 2 -induced HepG-2 cells. Furthermore, the anti-inflammatory effect and molecular mechanism of the CE of N. Tangutorum Bobr. fruits were evaluated using the dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) mouse model. CE significantly restored the body weight reduction, colon shortening, DAI elevation, and histological score in DSS-induced UC mice ( P < 0.01). In addition, CE could remarkably decrease the levels of MPO, IL-1 β , TNF- α , and IL-6 and increase the levels of superoxide dismutase, catalase, glutathione, and IL-10 in the colon of DSS mice ( P < 0.01). According to western blot analysis, CE inhibited the MAPK/NF- κ B signalling pathway activation. The results indicated that CE exerts a protective effect on DSS-induced UC mice, which may be related to the MAPK/NF- κ B signalling pathway activation. In conclusion, CE can be used as a therapeutic drug for UC.
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